Angina

What is the lung threshold? Congenital malformations of the lungs in children

It is possible to detect a tumor in the lungs and determine what it may be with a detailed examination. People of different ages are susceptible to this disease. Formations arise due to disruption of the process of cell differentiation, which can be caused by internal and external factors.

Neoplasms in the lungs are a large group of different formations in the lung area, which have a characteristic structure, location and nature of origin.

Neoplasms in the lungs can be benign or malignant.

Benign tumors have different genesis, structure, location and different clinical manifestations. Benign tumors are less common than malignant tumors and make up about 10% of the total. They tend to develop slowly and do not destroy tissue, since they are not characterized by infiltrating growth. Some benign tumors tend to transform into malignant ones.

Depending on the location there are:

Central - tumors from the main, segmental, lobar bronchi. They can grow inside the bronchus and surrounding lung tissue.
Peripheral - tumors from surrounding tissues and walls of small bronchi. They grow superficially or intrapulmonarily.

Types of benign tumors

There are the following benign lung tumors:

Briefly about malignant tumors

Increase.

Lung cancer (bronchogenic carcinoma) is a tumor consisting of epithelial tissue. The disease tends to metastasize to other organs. It can be located in the periphery, the main bronchi, or grow into the lumen of the bronchus or organ tissue.

Malignant neoplasms include:

Lung cancer has the following types: epidermoid, adenocarcinoma, small cell tumor.
Lymphoma is a tumor that affects the lower respiratory tract. It may occur primarily in the lungs or as a result of metastases.
Sarcoma is a malignant formation consisting of connective tissue. Symptoms are similar to those of cancer, but develop more quickly.
Pleural cancer is a tumor that develops in the epithelial tissue of the pleura. It can occur primarily, and as a result of metastases from other organs.

Risk factors

The causes of malignant and benign tumors are largely similar. Factors that provoke tissue proliferation:

Smoking active and passive. 90% of men and 70% of women who have been diagnosed with malignant tumors in the lungs are smokers.
Contact with hazardous chemicals and radioactive substances due to professional activities and environmental pollution in the area of residence. Such substances include radon, asbestos, vinyl chloride, formaldehyde, chromium, arsenic, and radioactive dust.
Chronic respiratory diseases. The development of benign tumors is associated with the following diseases: chronic bronchitis, chronic obstructive pulmonary disease, pneumonia, tuberculosis. The risk of malignant neoplasms increases if there is a history of chronic tuberculosis and fibrosis.

The peculiarity is that benign formations can be caused not by external factors, but by gene mutations and genetic predisposition. Malignancy and transformation of the tumor into malignant also often occur.

Any lung formations can be caused by viruses. Cell division can be caused by cytomegalovirus, human papillomavirus, multifocal leukoencephalopathy, simian virus SV-40, and human polyomavirus.

Symptoms of a tumor in the lung

Benign lung formations have various signs that depend on the location of the tumor, its size, existing complications, hormonal activity, the direction of tumor growth, and impaired bronchial obstruction.

Complications include:

abscess pneumonia;
malignancy;
bronchiectasis;
atelectasis;
bleeding;
metastases;
pneumofibrosis;
compression syndrome.

Bronchial patency has three degrees of impairment:

1st degree – partial narrowing of the bronchus.
2nd degree – valvular narrowing of the bronchus.
3rd degree – occlusion (impaired patency) of the bronchus.

Symptoms of the tumor may not be observed for a long time. The absence of symptoms is most likely with peripheral tumors. Depending on the severity of the symptoms, several stages of the pathology are distinguished.

Stages of formations

Stage 1. It is asymptomatic. At this stage, partial narrowing of the bronchus occurs. Patients may have a cough with a small amount of sputum. Hemoptysis is rare. During examination, the x-ray does not reveal any abnormalities. Studies such as bronchography, bronchoscopy, and computed tomography can show the tumor.

Stage 2. Valve narrowing of the bronchus is observed. At this point, the lumen of the bronchus is practically closed by the formation, but the elasticity of the walls is not impaired. When you inhale, the lumen partially opens, and when you exhale, it closes with the tumor. In the area of the lung that is ventilated by the bronchus, expiratory emphysema develops. As a result of the presence of bloody impurities in the sputum and swelling of the mucous membrane, complete obstruction (impaired patency) of the lung may occur. Inflammatory processes may develop in the lung tissues. The second stage is characterized by a cough with the release of mucous sputum (pus is often present), hemoptysis, shortness of breath, increased fatigue, weakness, chest pain, fever (due to the inflammatory process). The second stage is characterized by alternation of symptoms and their temporary disappearance (with treatment). An X-ray image shows impaired ventilation, the presence of an inflammatory process in a segment, lobe of the lung, or an entire organ.

To be able to make an accurate diagnosis, bronchography, computed tomography, and linear tomography are required.

Stage 3. Complete obstruction of the bronchial tube occurs, suppuration develops, and irreversible changes in lung tissue and their death occur. At this stage, the disease has such manifestations as impaired breathing (shortness of breath, suffocation), general weakness, excessive sweating, chest pain, elevated body temperature, cough with purulent sputum (often with bloody particles). Sometimes pulmonary hemorrhage may occur. During examination, an x-ray may show atelectasis (partial or complete), inflammatory processes with purulent-destructive changes, bronchiectasis, and a space-occupying lesion in the lungs. To clarify the diagnosis, a more detailed study is necessary.

Symptoms

Symptoms of low-quality tumors also vary depending on the size, location of the tumor, the size of the bronchial lumen, the presence of various complications, and metastases. The most common complications include atelectasis and pneumonia.

At the initial stages of development, malignant cavitary formations that arise in the lungs show few signs. The patient may experience the following symptoms:

general weakness, which intensifies as the disease progresses;
increased body temperature;
fatigue;
general malaise.

Symptoms of the initial stage of neoplasm development are similar to those of pneumonia, acute respiratory viral infections, and bronchitis.

The progression of a malignant formation is accompanied by symptoms such as cough with sputum consisting of mucus and pus, hemoptysis, shortness of breath, and suffocation. When the tumor grows into the vessels, pulmonary hemorrhage occurs.

A peripheral lung mass may not show signs until it invades the pleura or chest wall. After this, the main symptom is pain in the lungs that occurs when inhaling.

In later stages, malignant tumors appear:

increased constant weakness;
weight loss;
cachexia (depletion of the body);
the occurrence of hemorrhagic pleurisy.

Diagnostics

To detect tumors, the following examination methods are used:

Fluorography. A preventive diagnostic method, x-ray diagnostics, which allows you to identify many pathological formations in the lungs. read this article.
Plain radiography of the lungs. Allows you to identify spherical formations in the lungs that have a round outline. An x-ray image reveals changes in the parenchyma of the examined lungs on the right, left or both sides.
Computed tomography. Using this diagnostic method, the lung parenchyma, pathological changes in the lungs, and each intrathoracic lymph node are examined. This study is prescribed when differential diagnosis of round formations with metastases, vascular tumors, and peripheral cancer is necessary. Computed tomography allows a more accurate diagnosis to be made than x-ray examination.
Bronchoscopy. This method allows you to examine the tumor and perform a biopsy for further cytological examination.
Angiopulmonography. It involves performing invasive radiography of blood vessels using a contrast agent to detect vascular tumors of the lung.
Magnetic resonance imaging. This diagnostic method is used in severe cases for additional diagnostics.
Pleural puncture. Study in the pleural cavity with a peripheral tumor location.
Cytological examination of sputum. Helps determine the presence of a primary tumor, as well as the appearance of metastases in the lungs.
Thoracoscopy. It is carried out to determine the operability of a malignant tumor.

Fluorography.

Bronchoscopy.

Angiopulmonography.

Magnetic resonance imaging.

Pleural puncture.

Cytological examination of sputum.

Thoracoscopy.

It is believed that benign focal formations of the lungs are no more than 4 cm in size; larger focal changes indicate malignancy.

Treatment

All neoplasms are subject to surgical treatment. Benign tumors must be immediately removed after diagnosis in order to avoid an increase in the area of affected tissue, trauma from surgery, the development of complications, metastases and malignancy. For malignant tumors and benign complications, a lobectomy or bilobectomy may be required to remove a lobe of the lung. With the progression of irreversible processes, a pneumonectomy is performed - removal of the lung and surrounding lymph nodes.

Bronchial resection.

Central cavity formations localized in the lungs are removed by resection of the bronchus without affecting the lung tissue. With such localization, removal can be done endoscopically. To remove tumors with a narrow base, a fenestrated resection of the bronchial wall is performed, and for tumors with a wide base, a circular resection of the bronchus is performed.

For peripheral tumors, surgical treatment methods such as enucleation, marginal or segmental resection are used. For large tumors, lobectomy is used.

Lung formations are removed using thoracoscopy, thoracotomy and videothoracoscopy. During the operation, a biopsy is performed, and the resulting material is sent for histological examination.

For malignant tumors, surgical intervention is not performed in the following cases:

when it is not possible to completely remove the tumor;
metastases are located at a distance;
impaired functioning of the liver, kidneys, heart, lungs;
The patient's age is more than 75 years.

After removal of the malignant tumor, the patient undergoes chemotherapy or radiation therapy. In many cases, these methods are combined.

Covers a spectrum of cystic and adenomatous formations in the lobes, which are hamartomas with a cystic structure.

Exclude concomitant organ defects (up to 20%): kidneys, small intestine, diaphragmatic hernia, hydrocephalus, skeletal anomalies.

Prenatal diagnosis: polyhydramnios (compression of the esophagus or direct communication of the cyst with the respiratory tract) or dropsy (heart failure due to impaired venous return).

Diagnosis: Chest x-ray - multiple discrete blisters are visible, often with fluid levels within a single lobe.

First aid: consultation with a surgeon, planning the operation. With a prenatal diagnosis - as early as possible.

Beware pulmonary hypertension of a healthy lung.

Congenital lobar emphysema

Congenital lobar emphysema: almost always an emergency condition with overinflation of one lobe of the lung (without emphysematous destruction of lung tissue).

Causes: malformations of cartilage, bronchial tree, stenosis or external compression (vascular abnormality or tumor), polyalveolar lobe.

Caution: Always rule out mucus (meconium) plug as the cause (bronchoscopy).

Complications/problems: displacement, compression and excess blood flow in healthy lung tissue.

First aid: observation → surgery. Emergency surgery (lobectomy) is rarely required.

Lung sequestration

Lung sequestration: cystic or homogeneous area, in most cases in the lower lobes, usually on the left. This is a non-functional tissue not associated with the bronchial system. The blood supply comes most often from the aorta. Venous drainage can be into the systemic or pulmonary veins. They develop from an accessory lung bud from the foregut. The earlier the defect is formed, the more often the lung and sequestrum have a common pleura.

Increased likelihood of associated defects.

Complications: enlarged left-to-right shunt and, as a result, heart failure (> 80% of anastomoses with vessels of the esophagus or fundus of the stomach).

Prenatal diagnosis: Ultrasound.

Diagnostics, after birth, X-ray, if necessary, CT, angiography (MRI angiography) and scantigraphy with methylene diphosphonate (accumulation in the sequestrum).

Treatment: the method of choice is surgery, even in the absence of a clinic due to the risk of infection. Before surgery - treatment according to the clinical picture.

Agenesis and aplasia of the lungs

Bilateral agenesis is an extremely rare defect that is incompatible with life. Sometimes the trachea is also missing. Bronchial arteries and veins are usually absent. May be combined with defects of the esophagus, face and asplenia. A unilateral process is much more common; in 50-60% of patients, other congenital defects are observed: of the heart, genitourinary system, vertebrae and ribs, diaphragmatic hernia, etc. The only lung is compensatory enlarged. Bronchiectasis is often found in it.

Pulmonary hypoplasia (small lung)

Pulmonary hypoplasia occurs in 10% of childhood autopsies and in 85% of cases is combined with other congenital defects. Clinically characterized by the development of SDR, the severity of which depends on the degree of hypoplasia. Congenital pulmonary hypoplasia can be primary, or idiopathic, and secondary (much more often), unilateral and bilateral. Primary pulmonary hypoplasia is caused by genetic factors. It has been described in trisomies 13, 18 and 21, some genetic syndromes, in twins, and family cases are known.

Causes of secondary hypoplasia:

abnormalities of the vessels supplying the lung (pulmonary stenosis, tetralogy of Fallot, etc.);
oligohydramnios;
compression of the lungs by intrathoracic masses (congenital diaphragmatic hernia, congenital hydrops fetalis);
compression of the lungs due to chest deformities (asphyxial thoracic dystrophy, severe scoliosis);
lack of respiratory movements in the uterus due to neuromuscular diseases.

The diagnosis of idiopathic pulmonary hypoplasia is made in the absence of all the above reasons. The pathological anatomy of both forms of hypoplasia is the same. Macroscopically: both lungs may be uniformly reduced, or there is pronounced asymmetry (for example, with a diaphragmatic hernia). In cases where hypoplasia is the direct cause of death, lung weight is reduced by more than 40% and is often only 20-30% of normal weight for gestational age. Normally, full-term fetuses and newborns have a lung weight of -50 g. The indicator of relative lung weight is of greater importance for determining hypoplasia, i.e. ratio of lung weight to fetal weight. Normally, in fetuses and newborns 28 weeks of pregnancy and older, this figure is 0.012, in premature infants up to 28 weeks - 0.015 (interpreting the indicator of relative lung mass, it is necessary to take into account that in the presence of pathological processes in the lungs, such as pneumonia, HD, aspiration syndromes, etc., the relative weight will be higher). Depending on the microscopic picture, two main forms of pulmonary hypoplasia are distinguished. In the first case, the lungs are small, but in terms of maturity they correspond to gestational age, although the number of alveoli is reduced; in the second case, pronounced immaturity of the lung tissue is observed. This form is combined with oligohydramnios. Special staining reveals the absence of elastic tissue in the interlobar septa. Immunohistochemically, a significant decrease in the amount of type IV collagen is determined. Morphometric studies show that, regardless of the cause, the alveolar radial count is reduced in the hypoplastic lung. Alveolar radial count is easily determined on histological preparations by the number of alveolar septa located on a straight line drawn perpendicularly from the terminal bronchiole to the pleura or lobular septum. In full-term infants, the normal radial alveolar count is 4.1-5.3. Another method for determining hypoplasia is to measure the amount of lung DNA as an indicator of the total cell population of the lungs.

Pulmonary hyperplasia

More often it is a secondary defect. Lung enlargement is observed in cystic-adenomatous lung defects, congenital emphysema, as a compensatory process for unilateral agenesis or hypoplasia. True hyperplasia is always a bilateral process caused by obstruction in the upper respiratory tract. Lung hyperplasia in combination with laryngeal atresia is observed in autosomal recessive Fraser syndrome, characterized by cryptophthalmos, abnormalities of the ears, kidneys, syndactyly and cryptorchidism. Macroscopically: with a pronounced increase in the lungs, the diaphragm is shifted downwards, the lungs have imprints of the ribs, the relative weight is increased. Microscopically: more mature lung tissue with an increase in alveolar surface compared to the weight of the newborn and the gestational age. Hyperplasia of the lung with laryngeal atresia is caused by the lack of outflow of fluid from the lungs into the amnion cavity due to obstruction.

Accessory lung (tracheal accessory lung)

This extremely rare defect is caused by a violation of the division of the primary bronchial kidneys. It is necessary to differentiate with pulmonary sequestration and with “tracheal bronchus”.

Horseshoe lung

Refers to rare defects in which the lungs are partially connected by their bases behind the heart and in front of the esophagus. In the absence of other defects, it is asymptomatic, but it has been described in combination with various vascular anomalies of the lungs and other defects, such as hypoplasia of the right or left lung and scimitar syndrome.

Ectopic pulmonary tissue

There may be ectopic pulmonary tissue in the neck, abdominal cavity and chest wall, often combined with skeletal abnormalities and diaphragmatic hernia. Sometimes ectopic lung tissue in the abdominal cavity is referred to as extralobar sequestration. Neck ectopia is observed with inioncephaly, Klippel-Feil anomaly and cry-the-cat syndrome. The causes of pulmonary ectopia are not known.

Heterotopias in the lungs

Heterotopias have been described in the form of islands of tissue of the adrenal glands, pancreas, thyroid gland (without C-cells), liver, striated muscles, which are also found in pulmonary sequestra and hypoplastic lung. Their significance is small, since such heterotopias are observed only in children with other severe defects, mainly of the heart. In case of anencephaly, foci of glial tissue may enter the lung through the bloodstream or during ingestion. As a result of birth trauma, emboli from cerebellar tissue can be observed in the vessels, which are sometimes mistaken for hamartomas or heterotopic tissue.

Cystic lung disease

The existing classification of cystic lung disease is far from ideal. Currently, a distinction is made between congenital and acquired cysts. Acquired cysts in infants can be a consequence of infection, compression of the bronchus by an enlarged pulmonary artery, the presence of a foreign body in the bronchus, or bronchial hypoplasia. We do not consider them in this section. Congenital cysts include: bronchogenic cysts, pulmonary sequestration, cystic adenomatous lung disease, polyalveolar lobe, congenital lobar emphysema, lymphangiomatous cysts and enterogenic cysts.

Congenital lung cysts.

Rare vice

Cysts are single or multiple, always associated with the bronchial tree (postnatally often filled with fluid), limited to one lobe.

Differential diagnosis: pneumothorax.

Treatment: surgery is the method of choice. For tense cysts, they can be punctured as an emergency measure. Increase in size and tension can occur very quickly.

Bronchogenic cysts- These are congenital cystic formations. caused by impaired development of the primary intestine. They are usually located in the mediastinum near the carina of the trachea (51%), but can be located in the right paratracheal region, along the esophagus, at the hilum of the lung, or in various other locations. Bronchogenic cysts are rarely connected to the tracheobronchial tree or located in the lung tissue. In newborns they are asymptomatic or can cause SDR. Macroscopically: a round cyst with a smooth or rough internal surface, 1-4 cm in diameter, attached to the tracheobronchial tree, but not connected to it. The contents are a clear serous fluid, in cases of infection it is cloudy or bloody. Microscopically: the cyst is lined with ciliated cubic or columnar epithelium, sometimes squamous metaplasia is observed. The wall consists of a small amount of connective tissue, smooth muscle, pockets of cartilage and rarely bronchial glands. Bronchogenic cysts are combined with pulmonary sequestration, an additional lobe of the lung, described in Down syndrome.

Extralobar sequestration diagnosed in infants under 1 month of age. The ratio of boys: girls is 4: 1. Macroscopically: an isolated area of the lung with its own pleura, often cystically changed. It is located anywhere - from the neck to the diaphragm, most often behind the left lower lobe, and a diaphragm defect is often detected. May be located deep in the diaphragm or pericardium. About 15% of extralobar sequestra are localized in the abdominal cavity, sometimes connecting to the esophagus or stomach. Microscopically: among the pockets of normally formed alveoli there are small but dilated bronchi containing cartilage; in some cases, the dilation of the bronchi is more pronounced, and the alveoli are underdeveloped. Bronchioles and alveolar ducts are irregular in shape. The bronchi are not connected to the tracheobronchial tree. Lymphatic vessels are dilated, which resembles congenital lymphangiectasias. Arterial vessels have a normal structure, but thin-walled vessels can also be found. Due to the lack of normal drainage of the bronchi, secretions stagnate in them, which contributes to infection, cyst formation and fibrosis. Extralobar sequestration can be combined with cystic adenomatous lung disease, types II and III. In 65% of cases, defects of other organs are observed, the most common of which are diaphragmatic hernia, pulmonary hypoplasia, congenital heart disease and pectus excavatum. TTP defect - up to the 6th week of embryonic development.

At intralobar sequestration the abnormal area is usually located in the posterointernal parts of the lower lobe of the left lung among normal lung tissue and is not delimited from the surrounding parenchyma. Rarely combined with other PRs. It is extremely rarely diagnosed in newborns. Occurs with equal frequency in boys and girls. Macroscopically: the abnormal area appears as an atelectatic segment or as polycystic tissue, the cysts are filled with a yellowish-whitish clear fluid or jelly-like masses. Microscopically: the cysts are lined with columnar or cubic epithelium, the lung tissue is underdeveloped. In older children and adults, chronic inflammation with bronchiectasis, fibrosis, and cysts is observed in this area, on the basis of which many authors believe that in older age this is usually an acquired process and rarely congenital.

Infantile (congenital) lobar emphysema (congenital large supertransparent lobe) characterized by stretching of a segment or lobe of the lung due to internal or external obstruction of the bronchi. Boys get sick more often. Clinically diagnosed in newborns with SDD and infants, extremely rarely in older children (acquired emphysema must be excluded), and can cause death. The upper lobes are predominantly affected, rarely - two lobes. The causes of the defect are: stenosis, atresia, abnormal discharge of the bronchi, defects in the development of bronchial cartilage, mucous folds, mucus plugs and aspirated meconium in the bronchial lumen, obstruction of the bronchi by aberrant vessels or bronchogenic cysts, etc. These changes contribute to overstretching of the lung area distal to the site of obstruction due to the fact that when exhaling, less air is removed than enters (valve mechanism). Macroscopically: the affected lobe is enlarged; with sharp swelling, it prolapses through the anterior mediastinum towards the healthy lung, compressing neighboring areas. Microscopically: uniformly overstretched acini with alveolar sacs and alveoli measuring 3-10 times larger than normal are visible, focal ruptures in the alveolar septa are noted. In some cases, this type of emphysema is caused by an increase in the number of alveoli (3-5 times more than normal) in the affected lobe (polyalveolar lobe), while the size of the alveoli does not change. Infantile lobar emphysema is often combined with other defects, especially of the heart. Acquired infantile emphysema is observed in premature infants who were on mechanical ventilation.

Congenital cystic adenomatous lung defect (cystic adenomatous pulmonary dysplasia, cystic adenomatous pulmonary hamartoma)- quite common (accounts for 25% of all congenital lung diseases) hamartomatous lung defect, characterized by the presence of adenomatous proliferating cysts, reminiscent of bronchioles in structure. Cysts are usually connected to the tracheobronchial tree, the blood supply and venous outflow are carried out by normal pulmonary vessels, except in cases of combination with extralobar sequestration. The defect was first described by Ch"in and Tang in 1949. Frequency is 1 case per 25,000-35,000 births. In most cases, it is diagnosed in the first 6 months of life, in 70% - from birth or in the 1st month of life, occasionally later Almost 90% of all observations described in the literature were clinically manifested in children under 2 years of age. In 80% of cases, SDR is clinically observed in varying degrees of severity; in older children, persistent or recurrent pneumonia is present. Currently, the defect is often diagnosed antenatally. mainly in fetuses 22.6 ± 3 weeks of pregnancy, however, observations in 5-8-week fetuses are described. With antenatal diagnosis, this defect must be differentiated from diaphragmatic hernia, bronchogenic cysts, pulmonary sequestration and congenital lobar emphysema.

The etiology and pathogenesis of this defect are unknown. It is assumed that disruption of normal lung maturation may be due to bronchial atresia or abnormal bronchial division. This leads to dysplasia of the lung tissue distal to the affected segment. The formation of dysplastic lung tissue in the fetus can cause lung hypoplasia or even aplasia. Unlike a normally developing lung, with cystic adenomatous dysplasia there is an increase in cell proliferation and a decrease in the process of apoptosis. In the affected tissue, both in the fetus and in newborns, the expression of some growth factors is increased, in particular platelet-derived growth factor (TFR-BB), glial neurotropic factor (GNTF -GDNF), which are known to be some of the factors that stimulate lung growth and development, and the expression of GDNF in the affected tissue correlates with the degree of proliferation. There is also disintegration in the embryonic period between paracrine factors.

Depending on the clinical manifestations, prognosis and morphology, five types of defect are distinguished.

Type 0 - acinar dysplasia - a defect incompatible with life. Combined with heart defects and dermal dysplasia. Macroscopically: the lungs are small, dense, and when cut, the cysts resemble slightly dilated small bronchi. Microscopically: among the abundant mesenchyme there are small (0.5 cm in diameter) bronchiole-like structures lined with high columnar epithelium with mucus-producing goblet cells (mucosal differentiation is unique for this type of defect); the fibromuscular wall contains cartilage and glands.
Type I - cystic dysplasia - the most common type (50-75%). It is diagnosed in the 1st week or month of life, but can occur in older children and even adults. Macroscopically: one or many multilocular large cysts (diameter 3-10 cm), filled with air and fluid, surrounded by smaller cysts and compressed normal lung parenchyma. Microscopically: larger cysts are lined with ciliated, pseudomulti-row cylindrical, and smaller cysts are lined with cuboidal or columnar epithelium. In 1/3 of cases, there are mucus-producing cells in the epithelial lining of large cysts or in bronchiolo-alveolar-like structures near the largest cysts. Sometimes, within the cysts and in the adjacent bronchiole-like structures, papillary proliferation of the epithelium is observed, which resembles bronchogenic carcinoma. The wall of cysts consists of elastic, smooth muscle and collagen tissues; in 5-10% of cases cartilage is detected. It is usually treated surgically with a favorable prognosis.
Type II - intermediate - the second most common type (about 20-25%). It is observed only in the 1st year of life, has a worse prognosis and is more often combined with other congenital malformations of the heart, central nervous system, urinary, musculoskeletal systems, diaphragmatic hernia, some of them are incompatible with life (for example, arenia, sirenomelia). This type of defect is observed with extralobar sequestration. Macroscopically: the affected part or the entire lung on the section has a spongy appearance and consists of small cysts closely adjacent to each other with a diameter of 0.5 to 2 cm, connecting to the bronchi and filled with air if the child was breathing. The inner surface of the cysts is smooth, shiny or rough. They are evenly distributed among the lung tissue, merging with it. Microscopically: cysts resemble dilated terminal bronchioles, lined with respiratory cubic or columnar epithelium; the wall contains fibrous, elastic and smooth muscle fibers. Mucinous cells and cartilage are absent, but in 5-10% of cases there may be foci of striated muscles (rhabdomyomatous subvariant).
Type III - solid - occurs infrequently (5%) and almost only in boys. Pregnancy is complicated by polyhydramnios due to compression of the esophagus by enlarged lobes or the lung. With prolonged compression of the inferior vena cava, hydrops fetalis occurs. In the mother's blood in the 2nd trimester of pregnancy, an increase in the amount of α-feto-protein is observed. Macroscopically: large, dense, tumor-like masses occupy the entire lobe or the entire lung, the mediastinum is always displaced and the affected lung is often hypoplastic (cystic pulmonary hypoplasia). The section reveals small cavities resembling cysts, rarely more than 0.2 cm in diameter (except for scattered, larger bronchiole-like structures). The pulmonary parenchyma outside the cysts is underdeveloped. Microscopically: the affected tissue resembles an immature lung devoid of bronchi. Irregular stellate bronchiole-like structures are lined with cuboidal epithelium and surrounded by alveolar ducts and alveoli, also lined with cuboidal epithelium. Mucous cells and cartilage are absent. The cysts observed in the types described above are absent. The prognosis depends on the extent of the process and the amount of preserved lung tissue, the degree of mediastinal displacement and the presence of congenital malformation. Mortality is high.
Type IV - peripheral cystic, distal acinar - occurs in 2-10% of cases. Boys and girls are affected equally often. It is observed in newborns and small children of the first 4 years of life. Macroscopically: large, multilocular, thin-walled, air-containing cysts are localized at the periphery of the lung and can compress other organs of the chest, occasionally complicating pneumothorax. Microscopically, the cysts are lined with flattened alveolar epithelium (type I alveolocytes). The wall consists of dense mesenchymal tissue with clearly visible arteries and arterioles. Mucous cells, cartilage and muscles are absent. The prognosis for surgical treatment is favorable.

Congenital pulmonary lymphangiectasias (lymphangiomatous cysts) are primary and secondary. Secondary ones are caused by obstruction of lymphatic or venous drainage of the lungs, primary ones are an extremely rare defect. Boys are affected 2 times more often. The reasons are heterogeneous. They can be inherited autosomal recessively, but in most cases the defect is sporadic. Often combined with other congenital defects, especially asplenia and heart defects, they are described in Noonan, Turner and Down syndromes. Primary pulmonary lymphangiectasias can be isolated (only the lung is affected) or a manifestation of generalized lymphangiectasias. In newborns, pronounced SDR is clinically observed. In most cases, death occurs within the first hours or days of life, but occasionally they may be first clinically diagnosed only in adults. Macroscopically: the lungs are enlarged, dense, tuberous. In the wide interlobar septa and under the pleura, multiple cysts with a diameter of up to 5 mm are visible, emphasizing the lobar structure of the lungs. Near the hilum of the lungs there are oblong cysts. The contents of the cysts are lymph, or when connected to the bronchi - air and lymph. Microscopically: cysts are localized in the connective tissue under the pleura, in the interlobar septa, near the bronchioles and arteries. Serial sections show that they are part of a complex network of interconnecting lymphatic channels that vary widely in size and lack valves. The cysts are lined with flattened endothelium (markers of the endothelium of lymphatic vessels are CD 31 and factor 8 antigens). In the thin wall, elastic, collagen fibers and rarely smooth muscle cells are detected. The absence of foreign body giant cells in the cyst wall distinguishes this pathology from persistent interstitial emphysema, which is usually a complication of mechanical ventilation in premature infants.

Enterogenous cysts is a form of single-chamber duplication cysts of the gastrointestinal tract. In the chest cavity they are localized in the posterior mediastinum on the right, attached to the esophagus, and rarely connected to the bronchus. Microscopically: the wall of the cyst is lined with multilayered squamous, occasionally gastric or small intestinal epithelium. The gastric epithelium may ulcerate, leading to perforation of the cyst. Enterogenous cysts can be combined with anomalies of the lower cervical and upper thoracic vertebrae.

Capillary alveolar dysplasia- disruption of the structure of the pulmonary vessels. A rare lethal pathology that causes congenital pulmonary hypertension, persistence of fetal circulation and SDR in newborns. Microscopically: the proliferation of connective tissue in the interlobar and interalveolar septa, in which the number of capillaries is reduced, there is no contact between the alveolar epithelium and the capillary. The pulmonary lobules are small, the radial count is reduced. The walls of small arteries are thickened due to hypertrophy of smooth muscle tissue. In addition, there is an abnormal arrangement of the pulmonary veins, which accompany the pulmonary arteries in the center of the acinus, and not in the interlobar septa, as is observed in normal lung tissue. The walls of abnormally located veins are thickened. The causes of the defect are not known. Siblings are rarely affected. May be combined with gastrointestinal and urinary tract defects.

Pulmonary arteriovenous fistulas- abnormal communications between arteries and veins. The process is most often localized in the lower lobe. It is observed in 25% of patients with Randu-Weber-Osler disease (familial hemorrhagic telangiectasia) - an autosomal dominant hereditary disease with high penetrance. Homozygous forms are in some cases lethal in early childhood.

Congenital surfactant deficiency (congenital alveolar proteinosis)

This is an autosomal recessive hereditary deficiency of one of the surfactant proteins - surfactant protein B (SP-B), caused by a mutation in codon 121 of the SP-B gene and its RNA - SP-B mRNA. Clinically characterized by rapidly progressing respiratory failure immediately after birth. Macroscopically: the lungs are dense, more than 2 times enlarged, airless. Microscopically: the alveoli are dilated, lined with cuboidal epithelium and filled with eosinophilic, granular, PAS positive masses with desquamated alveolocytes and an abundance of macrophages. In the final stage, thickening of the alveolar septa is observed due to the proliferation of fibroblasts. Immunohistochemically, the absence or reduction of surfactant protein is determined with normal amounts of proteins A and C. The prognosis is unfavorable. In all cases described in the literature, death occurred within the 1st year of life.

Primary pulmonary hypertension

Hypertension of the pulmonary circulation in newborns can be associated with the persistence of the fetal arteries of the lungs, hypertrophy of their muscular layer, proliferation and fibrosis of the intima, sometimes fibrinoid necrosis and arteritis, which leads to precapillary obstruction of the branches of the pulmonary artery and the formation of secondary glomus anastomoses. With this variant, the disease occurs in a fulminant manner, and children die in the first months of life. Sudden death is often observed. Hypertrophy of the muscular lining of the pulmonary vessels (mainly small intraacinar arteries) is also observed with intrauterine asphyxia, pulmonary hypoplasia, premature closure of the ductus arteriosus, and diaphragmatic hernia.

Benign familial pneumothorax

It is extremely rare in newborns and is mainly observed in adolescent males. Families with both autosomal dominant and autosomal recessive types of inheritance have been described.

Among the many classifications of lung cancer, the classification based on anatomical and physiological data has become widespread. This classification distinguishes 5 forms of lung cancer: 1) central; 2) peripheral; 3) apical; 4) mediastinal and 5) miliary pulmonary carcinosis.

Central lung cancer. Clinical symptoms of the disease occur when bronchial obstruction is impaired and the drainage function of the bronchus changes. Basically, the patient's complaints boil down to the appearance of a cough, sometimes paroxysmal, sputum with blood, shortness of breath, general weakness, increased fatigue, increased body temperature to subfebrile levels, and loss of body weight.

Central cancer develops from the epithelium of the mucous membrane of large bronchi: main, lobar or segmental. Tumor growth can be directed into the lumen of the bronchus (mainly endobronchial cancer); peribronchial tumor growth, outward from the bronchial wall (mainly exobronchial cancer), is relatively rarely observed.

With endobronchial growth of a cancerous tumor in the initial phase of development, when the size of the tumor is very small, it is impossible to establish a diagnosis clinically and radiologically. As its size increases, the ventilation of a segment or lobe of the lung is impaired, which gives reason to suspect a tumor. The second phase of tumor development begins and the first stage of bronchostenosis development - hypoventilation. In this phase of tumor growth, functional tests should be used: with a sharp inspiration (positive Holtzknecht-Jacobson sign), the mediastinum shifts to the painful side, and with a cough impulse (positive Prozorov sign), the mediastinum shifts jerkily to the healthy side. In the second stage of bronchostenosis, valvular emphysema may develop, which is radiographically characterized by increased transparency of a segment or lobe, widening of the intercostal spaces, and displacement of the mediastinum during forced inspiration to the healthy side. As the tumor grows, complete blockage of the bronchial tube occurs - a violation of bronchial patency of the third stage, which leads to the development of atelectasis (Fig. 3.8). On X-ray examination, the collapsed segment, lobe or lung appears as a homogeneous intense shadow, their dimensions are reduced, the interlobar boundaries are concave, the diaphragm is high, and the mediastinum is shifted towards the lesion. When performing bronchography, a defect in the filling of the bronchus is detected, in the initial stages - unevenness, usurization of its contour, with complete obstruction - amputation of the bronchus.

Tomograms can detect a narrowing of the lumen of the bronchus, the shadow of a tumor, or a break in the air column of the bronchus when it is blocked by a tumor.

Exobronchial cancer. Changes in the root of the lung are determined, its expansion due to the tumor node and metastases to the lymph nodes, the root shadow loses its structure, merging with the median shadow. The contour facing the pulmonary field is radiant and stranded, which indicates tumor growth into the pulmonary tissue surrounding the root (Fig. 3.56, 3.57).

An increase in tumor size to several centimeters in diameter leads to a narrowing of the bronchial lumen and impaired ventilation.

Predominantly peribronchial growth of the tumor cannot be determined, since from the very beginning it spreads along the bronchus and blood vessels. As the tumor grows, thick muffs form, enlarge, and on x-rays, rough shadows are detected, fan-shaped, extending from the root into the lung tissue. Tomograms reveal uniform thickening of the bronchial walls. With further growth of the tumor and germination of the wall, the lumens of the bronchi narrow, and hypoventilation occurs. Bronchography reveals an extended concentric narrowing of the bronchi and thickening of their walls.

CT shows all components of the picture of central lung cancer better than radiography: bronchoconstriction, atelectasis, metastatic lymphadenopathy in the roots of the lungs and mediastinum. Intravenous contrast helps clarify the atelectatic nature of the pathological shadow in the lung, in which the collapsed lung often intensifies more intensely than the tumor.

On MRI, obstructive atelectasis has an intense signal on T2-weighted images and thus differs from a low-intensity tumor conglomerate.

Peripheral lung cancer develops from the wall of a small bronchus and most often grows in the form of a node, located either subpleurally or at a considerable distance from the pleura. The most common localization of peripheral cancer is noted in the right lung and the upper lobes of both lungs.

Clinically, peripheral cancer does not manifest itself for a long time, since it is located away from the large bronchi. In this regard, it is often determined radiographically. Clinical manifestations arise later and are characterized by the appearance of chest pain, which is caused by tumor growth into the pleura; when it grows into the bronchus, a cough with sputum production and hemoptysis appears. Peripheral cancer at the beginning of its development forms a small node of a polygonal shape, reaching a diameter of 3-4 cm, it acquires a spherical shape. Tumor growth is slow, sometimes fast. The intensity of the shadow may vary depending on the size of the node. The shadow is often heterogeneous, the contour is lumpy. The pulmonary pattern near the tumor node is usually deformed, which is apparently due to a previous chronic inflammatory process. In some cases, it is possible to see a path running from the round shadow of the tumor to the root of the lung, caused by lymphangitis or peribronchial and perivascular growth of the tumor.

Tomography used for peripheral cancer reveals the nodularity of the tumor shadow, the decay cavity, helps to identify the draining bronchus, the condition of the lymph nodes of the root of the lung and mediastinum (Fig. 3.58).

Apical lung cancer. Radiologically, apical cancer is characterized by a shadow that occupies the entire area of the apex of the lung. The lower border of the shadow is clear, convexly facing downwards, while the remaining borders are not differentiated. Against the background of the shadow, it is usually possible to see the destruction of the posterior segments of the ribs and transverse processes of several vertebrae.

Mediastinal form of cancer. In the clinical picture, the most important is compression syndrome (superior vena cava syndrome, compression of large nerve trunks). Swelling of the neck, face, and a feeling of tightness in the neck and chest appear. The primary localization of the tumor in most cases is unclear, the minimal size of the tumor does not allow it to be determined by X-ray examination, however, an early tendency to metastasize to the mediastinal lymph nodes is characteristic.

The leading method for diagnosing mediastinal formations is currently CT, which makes it possible to establish the exact localization of the formation, its relationship with surrounding anatomical structures, and in some cases give a fairly accurate tissue description of the formation (lipomas, cysts).

X-ray: a picture characteristic of a mediastinal tumor. The presence of extensive tissue covering the shadow of the lung root on one side (unilateral enlargement of the lymph nodes), merging with the median shadow. The contour of the shadow facing the pulmonary field corresponds to an uneven increase in groups of lymph nodes. It can be difficult to determine the nature of enlarged lymph nodes, because... A similar picture is given by lymphoproliferative diseases.

CT is a valuable modality for the clinical staging of lung cancer, more sensitive than radiography.

MRI helps to better recognize tumor invasion of the mediastinum and chest.

PET is significantly more accurate than CT in assessing solitary pulmonary nodules and in determining the stage of lung cancer.

Metastases of malignant tumors to the lungs. Typically, MTCs produce a circular shadow in the X-ray image. They are usually multiple, but sometimes solitary MTS are found. CT is the most sensitive method for detecting MTS in the lungs. It provides reliable recognition of nodules up to 3 mm in size (radiography > 6 mm); in the area of the roots of the lungs, the detection threshold for CT is 5-6 mm (Fig. 3.59 and 3.60).

Miliary carcinosis is expressed by small focal symmetrical dissemination, especially dense in the lower parts of the lungs. Differential diagnosis is difficult. It is necessary to conduct a thorough sputum analysis and sometimes a puncture biopsy.

Cancerous lymphangitis initially manifests itself as an enhanced and deformed pulmonary pattern with a looped mesh structure. Then, as a result of the progression of the tumor process, the lymph nodes and roots of the lungs enlarge, from which linear shadows extend radially.

Diseases of the lungs and bronchi are common. In recent years, there has been a steady trend towards an increase in the percentage of patients suffering from diseases of the bronchopulmonary system.

Symptomatically, such pathologies are expressed in two ways: either in the form of an acute severe process, or in the form of sluggish progressive forms. Neglect, improper treatment and the principle “it will go away on its own” lead to tragic consequences.

It is impossible to determine the cause of the disease at home. Only a qualified pulmonologist can diagnose the pathological process.

A distinctive feature of many pulmonary diseases is difficult diagnosis. The causes of a particular pathology may be subjective. But there are a number of common factors that provoke the occurrence and development of the inflammatory process:

unfavorable environmental situation in the region; presence of hazardous industries;
exacerbation of other chronic diseases;
pathologies of the cardiovascular system;
disturbance of electrolyte balance in the body, increased sugar levels;
nerve diseases;
presence of bad habits.

Each pathological process in the lungs has specific signs that appear as it develops. In the initial stages, the manifestations of all pulmonary diseases are very similar.

Presence of cough. A cough is the first sign of a possible lung disease. The pathological process provokes inflammation, irritation of receptors and reflex contraction of the muscles of the respiratory tract.
Coughing is the body’s natural attempt to get rid of accumulated mucus. Already by the timbre of the cough one can judge whether the patient has any pathology: croup, laryngotracheobronchitis, bronchiectasis.

During coughing attacks, the patient experiences:

discomfort;
pain and burning in the sternum;
lack of air;
pressing sensation in the chest.

Sputum production. As a consequence of the pathological process, sputum saturated with pathogenic microbes is considered. With inflammation, the amount of discharge increases significantly. The patient's disease is determined by the color of the sputum, its smell and consistency. An unpleasant odor indicates putrefactive processes in the lungs; white, foamy discharge is a sign of pulmonary edema.
Presencebloodin sputum orsaliva. Often serves as a sign of a dangerous disease. The cause may be damage to a small vessel, malignant neoplasms, or lung abscess. In any case, the presence of blood in sputum or saliva requires immediate referral to specialists.
Difficulty breathing. A symptom of almost all diseases of the bronchi and lungs. In addition to lung problems, it can be caused by dysfunction of the cardiovascular system.
Painful sensations in the sternum. Chest pain is a characteristic sign of pleural damage. It is most often found in various forms of pleurisy, cancer, and foci of metastases in the pleural tissues. Chronic pulmonary pathologies are considered as one of the prerequisites for pleurisy.

With infectious lesions of the lungs, symptoms appear suddenly and vividly. Fever appears almost immediately, there is a sharp increase in temperature, chills and profuse sweating.

Classification

A characteristic feature of pulmonary diseases is their effect not only on various parts of the lungs, but also on other organs.

According to the lesions, bronchopulmonary pathologies are classified by the following criteria:

lung diseases affecting the respiratory tract;
diseases affecting the alveoli;
pathological lesions of the pleura;
hereditary lung pathologies;
diseases of the bronchopulmonary system;
purulent processes in the lungs;
congenital and acquired lung defects.

Lung diseases affecting the airways

COPD(chronic obstructive pulmonary disease). In COPD, the bronchi and lungs are simultaneously affected. The main indicators are a constant cough, sputum production, shortness of breath. Currently, there are no therapeutic methods that completely cure the pathology. Risk groups include smokers and patients associated with hazardous production. At the third stage, the patient’s life expectancy is about 8 years, at the last stage - less than a year.
Emphysema. The pathology is considered a type of COPD. The disease is characterized by impaired ventilation, blood circulation and destruction of lung tissue. The release of carbon dioxide is characterized by significant and sometimes critical indicators. It occurs both as an independent disease and as a complication of tuberculosis, obstructive bronchitis, and silicosis. As a consequence of the pathology, pulmonary and right ventricular heart failure and myocardial dystrophy develop. The main symptoms for all types of emphysema are changes in skin color, sudden weight loss, and shortness of breath.
Asphyxia- oxygen starvation. Characterized by a lack of oxygen and an excess amount of carbon dioxide. There are two groups of asphyxias. Non-violent is considered as a serious consequence of bronchopulmonary and other diseases. Violent - occurs with mechanical, toxic, barometric lesions of the bronchi and lungs. With complete suffocation, irreversible changes and death occur in less than five minutes.
Acute bronchitis. When the disease occurs, the patency of the bronchi is impaired. Acute bronchitis is characterized by symptoms of both acute respiratory disease and intoxication. It can have either the form of a primary pathology or be the result of complications of other processes. Two common causes are damage to the bronchi by infection or viruses. Less common is acute bronchitis of an allergic nature.

Symptomatically expressed by a continuous cough, sputum production, and profuse sweating. Self-medication, improper use of medications, and untimely contact with specialists threaten the disease becoming chronic.

A typical manifestation of chronic bronchitis is a cough that occurs with any slight decrease in immune activity.

Alveolar pathologies

Alveoli are air sacs, the smallest part of the lung. They have the appearance of bubbles, the walls of which are also their partitions.

Lung pathologies are also classified by damage to the alveoli.

Pneumonia. An infectious disease caused by viruses or bacteria. When the disease is neglected, if it is not timely to contact a specialist, it turns into pneumonia.

A characteristic feature is the rapid, sometimes reactive development of pathology. At the first signs, immediate consultation with a doctor is required. Clinically expressed as follows:

heavy, “crispy” breathing;
a sharp and strong increase in temperature, sometimes to critical levels;
separation of sputum in the form of mucous lumps;
shortness of breath and chills;
in severe cases of the disease, a change in skin color is observed.

Tuberculosis. Causes severe processes in the lungs and, if immediate assistance is not provided, leads to the death of the patient. The causative agent of the pathology is Koch's bacillus. The danger of the disease is during a long incubation period - from three weeks to a year. To exclude infection, an annual examination is indicated. The initial stages of the disease are characterized by:

persistent cough;
low but not decreasing temperature;
the appearance of blood streaks in saliva and sputum.

Important. In children, the clinical picture is more pronounced, the disease is more severe, develops much faster and leads to the most dire consequences. Parents, first of all, should pay attention to the following signs:

the child has been coughing for more than 20 days;
loss of appetite;
decreased attention, fatigue and apathy;
signs of intoxication.

Pulmonary edema. It is not an independent disease and is considered a serious complication of other diseases. There are several types of pulmonary edema. The most common causes are either fluid entering the lung space or destruction of the outer walls of the alveoli by toxins produced by the human body itself.

Pulmonary edema is a dangerous disease that requires quick and accurate diagnosis and immediate treatment.

Lung cancer. Aggressive, rapidly developing oncological process. The last, terminal stage leads to the death of the patient.

Cure is possible at the very beginning of the disease, but few people will pay attention to a constant cough - the main and main symptom of the early stage of lung cancer. To detect the disease at the earliest stages, a computed tomography scan is necessary.

The main symptoms of the pathology are:

cough;
blood streaks and whole blood clots in the sputum;
dyspnea;
constantly elevated temperature;
sudden and significant weight loss.

Additional information. The longest life expectancy is observed in patients with peripheral lung cancer. There are officially registered cases where patients lived for 8 years or more. The peculiarity of pathology is its slow development in the complete absence of pain. Only in the terminal stage of the disease, with total metastasis, did patients develop pain.

Silicosis. Occupational disease of miners, miners, grinders. Grains of dust, tiny fragments of glass and stone settle in the light years. Silicosis is insidious - signs of the disease may not appear at all for many years, or may be mild.

The disease is always accompanied by a decrease in lung mobility and disruption of the respiratory process.

Tuberculosis, emphysema, and pneumothorax are considered severe complications. In the final stages, a person suffers from constant shortness of breath, cough, and fever.

Acute respiratory syndrome - SARS. Other names are SARS and purple death. The causative agent is coronavirus. It multiplies quickly and in the process of development destroys the pulmonary alveoli.

The disease develops over 2-10 days and is accompanied by renal failure. After discharge, the patients noted a proliferation of connective tissue in the lungs. Recent studies indicate the ability of the virus to block all parts of the body's immune response.

Pathological lesions of the pleura and chest

The pleura is a thin sac that surrounds the lungs and the inside of the chest. Like any other organ, it can be affected by disease.

With inflammation, mechanical or physical damage to the pleura, the following occurs:

Pleurisy. Inflammation of the pleura can be considered both as an independent pathology and as a consequence of other diseases. About 70% of pleurisy is caused by the invasion of bacteria: Legionella, Staphylococcus aureus and others. When infection penetrates, due to physical and mechanical damage, the visceral and parietal layers of the pleura become inflamed.

Characteristic manifestations of the disease are stabbing or dull pain in the sternum, severe sweating, and in severe forms of pleurisy - hemoptysis.

Pneumothorax. It occurs as a result of penetration and accumulation of air in the pleural cavity. There are three types of pneumothorax: iatrogenic (arising as a result of medical procedures); traumatic (as a result of internal damage or injury), spontaneous (due to heredity, lung defect or other disease).

Pneumothorax can lead to lung collapse and requires immediate medical attention.

Chest diseases are associated with pathological processes in the blood vessels:

Pulmonary hypertension. The first signs of the disease are associated with disturbances and changes in pressure in the main vessels of the lungs.

Important. The forecast is disappointing. 20 people out of a hundred die. The timing of the development of the disease is difficult to predict; it depends on many factors, and, above all, on the stability of blood pressure and the condition of the lungs. The most alarming sign is frequent fainting. In any case, the survival rate of patients, even with the use of all possible treatment methods, does not cross the five-year threshold.

Pulmonary embolism. One of the main reasons is vein thrombosis. The blood clot travels to the lungs and blocks oxygen flow to the heart. A disease that threatens sudden, unpredictable hemorrhage and death of the patient.

Permanent chest pain can be a manifestation of the following diseases:

Hyperventilation with excess weight. Excess body weight puts pressure on the chest. As a result, breathing becomes irregular and shortness of breath occurs.
Nervous stress. A classic example is myasthenia gravis, an autoimmune disease called muscle flaccidity. Considered as a pathological disorder of nerve fibers in the lungs.

Diseases of the bronchopulmonary system as a hereditary factor

The hereditary factor plays an important role in the occurrence of pathologies of the bronchopulmonary system. In diseases transmitted from parents to children, gene mutations provoke the development of pathological processes regardless of external influences. The main hereditary diseases are:

Bronchial asthma. The nature of occurrence is the effect of allergens on the body. It is characterized by shallow shallow breathing, shortness of breath, and spastic phenomena.
Primary dyskinesia. Congenital pathology of the bronchi of a hereditary nature. The cause of the disease is purulent bronchitis. Treatment is individual.
Fibrosis. Connective tissue grows and replaces alveolar tissue with it. As a result - shortness of breath, weakness, apathy in the early stages. In the later stages of the disease, the skin changes color, a bluish tint appears, and drumstick syndrome is observed - a change in the shape of the fingers.

The aggressive form of chronic fibrosis shortens the patient's life to one year.

Hemosiderosis. The reason is an excess of hemosiderin pigment, a massive release of red blood cells into the body tissues and their breakdown. Indicative symptoms are hemoptysis and shortness of breath at rest.

Important. Acute respiratory infection is the root cause of pathological processes in the bronchopulmonary system. The first symptoms of the disease do not cause anxiety or fear in patients; they are treated at home with traditional remedies. The disease enters a chronic phase or acute inflammation in both lungs.

Bronchopulmonary diseases are the result of viruses entering the body. Damage occurs to the mucous membranes and the entire respiratory system. Self-medication leads to serious consequences, including death.

The primary manifestations of diseases of the bronchi and lungs are practically no different from the symptoms of a common cold. Lung infections are bacterial in nature. The development of inflammatory processes occurs rapidly – sometimes taking several hours.

Diseases caused by bacteria include:

pneumonia;
bronchitis;
asthma;
tuberculosis;
respiratory allergies;
pleurisy;
respiratory failure.

The development of infection is reactive. To prevent life-threatening consequences, a full range of preventive and therapeutic measures is carried out.

Many bronchial and pulmonary pathologies are accompanied by sharp and severe pain and cause interruptions in breathing. Here, a treatment regimen specific to each patient is used.

Suppurative lung diseases

All suppurative lung diseases are classified as serious pathologies. The set of symptoms includes necrosis, putrefactive or purulent decay of lung tissue. Pulmonary purulent infection can be total and affect the entire organ, or be focal in nature and affect individual segments of the lung.

All purulent pathologies of the lungs lead to complications. There are three main types of pathologies:

Lung abscess. A pathogenic process in which lung tissue melts and is destroyed. As a result, purulent cavities are formed, surrounded by dead lung parenchyma. Pathogens: Staphylococcus aureus, aerobic bacteria, aerobic microorganisms. With a lung abscess, fever, pain in the inflamed segment, sputum with pus, and expectoration of blood are observed.

Treatment includes lymphatic drainage and antibacterial therapy.

If there is no improvement within two months, the disease becomes chronic. The most severe complication of a lung abscess is gangrene.

Lung gangrene. Total tissue decay, putrefactive pathogenic processes in the lungs. An obligatory accompanying symptom is sputum with an unpleasant odor. The fulminant form of the disease causes the patient’s death on the first day.

Symptoms of the disease include an increase in temperature to critical levels, heavy sweating, sleep disturbances, and a persistent cough. In severe stages of the disease, patients experienced changes in consciousness.

It is impossible to save a patient at home. And with all the successes of thoracic medicine, the mortality rate of patients with lung gangrene is 40-80%.

Purulent pleurisy. It is an acute purulent inflammation of the parietal and pulmonary membranes, and the process affects all surrounding tissues. There are infectious and non-infectious forms of pleurisy. The development of the disease is often reactive in nature; immediately initiated therapeutic measures can save the patient. The main symptoms of the pathology are:

shortness of breath and weakness;
pain on the side of the affected organ;
chills;
cough.

Congenital lung defects

A distinction should be made between congenital pathologies and congenital lung anomalies.

Abnormalities of the lungs do not manifest themselves clinically; the modified organ functions normally.

Developmental defects are a complete anatomical disorder of the structure of an organ. Such disorders occur during the formation of the bronchopulmonary system in the embryo. The main lung defects include:

Aplasia– a serious malformation in which either the entire organ or part of it is missing.
Agenesis– a rare pathology, there is a complete absence of the lung and main bronchus.
Hypoplasia– underdevelopment of the lungs, bronchi, lung tissue, blood vessels. The organs are in their infancy. If hypoplasia affects one or more segments, it does not manifest itself in any way and is discovered by chance. If everything is undeveloped, hypoplasia manifests itself in signs of respiratory failure.
Tracheobronchomegaly, Mounier-Kuhn syndrome. It occurs when the elastic and muscular structures of the bronchi and lungs are underdeveloped, as a result of which a gigantic expansion of these organs is observed.
Tracheobronchomalacia– a consequence of defects in the cartilage tissue of the trachea and bronchi. When you inhale, the lumen of the airways narrows, and when you exhale, it widens greatly. The consequence of the pathology is constant apnea.
Stenosis– reduction of the lumen of the larynx and trachea. There is a serious disruption of respiratory function and the swallowing process. The defect significantly reduces the patient’s quality of life.
Accessory lung lobe. In addition to the main pair of lungs, there are accessory lungs. They practically do not manifest themselves at all; clinical symptoms occur only during inflammation.
Severstation. A section of lung tissue is separated from the main organ, which has its own blood flow, but does not take part in the process of gas exchange.
Azygos vein. The right side of the lung is divided by the azygos vein.

Congenital defects are easily noticed on ultrasound, and modern courses of therapy make it possible to stop their further development.

Diagnostic methods and preventive measures

The more accurately the diagnosis is made, the faster the patient’s path to recovery. At the first examination, the pulmonologist must take into account all external manifestations of the disease and the patient’s complaints.

Based on the initial examination and conversation with the patient, a list of necessary examinations is compiled, for example:

X-ray;
fluorography;
blood test,
tomography;
bronchography;
testing for infections.

Based on the data obtained, an individual treatment regimen is determined, procedures and antibacterial therapy are prescribed.

But none of the most modern methods of treatment, none of the most effective drugs will bring any benefit if you do not follow all the prescriptions and recommendations of a specialist.

Preventive measures will significantly reduce the risk of pulmonary pathologies. The rules are simple, everyone can follow them:

avoiding smoking and excessive drinking of alcohol;
physical education and light physical activity;
hardening;
relaxation on the sea coast (and if this is not possible, walks in a pine forest);
annual visits to a pulmonologist.

The symptoms of pulmonary diseases described above are easy to remember. Every person should know them. Know and seek medical help at the first warning signs.