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Vascular pathology of the lungs.

Vascular pathology of the lungs occurs in various diseases of the lungs, heart and blood vessels, liver and is described by a variety of syndromes. The most important variants of pulmonary vascular pathology are represented by the following groups of diseases: pulmonary edema; adult respiratory distress syndrome; pulmonary embolism syndrome; syndromes of primary and secondary pulmonary hypertension; pulmonary vasculitis; pulmonary hemorrhages and heart attacks.

Pulmonary edema. Pulmonary edema complicates many diseases of the lungs, heart, and other organs. In the tissue of the edematous lung, more than 4-5 ml of fluid is accumulated per gram of dry matter.

The mechanism of development of pulmonary edema is associated with an imbalance between three components: hydrostatic intracapillary pressure, oncotic pressure, vascular-tissue permeability, and lymphatic drainage. In this case, with the development of pulmonary edema, an increase in the performance of one or more of the first three components is noted and, on the contrary, a decrease in the work of lymphatic drainage.

Pulmonary edema is most often caused by two groups of reasons: an increase in hydrostatic pressure in the venous part of the pulmonary circulation (with acute left ventricular failure, mitral stenosis, hypervolemia of the pulmonary circulation, obstruction of the pulmonary veins) or a local increase in the permeability of capillaries of the alveolar septum (with adult respiratory distress syndrome )

In addition, pulmonary edema can develop with a decrease in blood oncotic pressure with nephrotic syndrome, liver diseases, enteropathy, accompanied by hypoalbuminemia, as well as edema caused by obstruction of lymphatic drainage.

The clinical picture of pulmonary edema is characterized by the development of shortness of breath, orthopnea, cough, sometimes with a pink foamy type of sputum. During auscultation, crepitus is found in the basal parts of the lung. Functional tests demonstrate a decrease in lung capacity, hypoxemia, hypercapnia. A vascular pattern with vasodilatation and fluid levels in the lungs are radiologically detected (Curly B line).

The morphology of pulmonary edema consists of micro- and macroscopic manifestations. Macroscopically light red, heavy and wet. When pressed, a foamy red liquid flows from the surface of the incision. Microscopically, pulmonary edema has different manifestations depending on the stage. In the first stage, the edematous fluid accumulates in the interstitial tissue of the lung, in the second - in the lumen of the alveoli, which becomes possible only when the tight contacts between the first order pneumocytes are destroyed with a sharp increase in the pressure of the interstitial edematous fluid. With the progression of edema, red blood cells and other cellular elements of the blood go into the lumen of the alveoli.

Pulmonary edema can resolve without any consequences. However, interstitial fibrosis often develops in the outcome, and with chronicity of the process, sclerosis and hemosiderosis of the lungs.

Adult respiratory distress syndrome. In the literature, adult respiratory distress syndrome (RDSV) is described under different names: shock lung, diffuse damage to the alveoli, acute damage to the alveoli, traumatic wet lung. The clinical picture and morphological changes in RDSV are similar to those in newborn respiratory distress syndrome, which gave the name to this suffering. However, neonatal ECD has a different etiology and pathogenesis.

RDSV (from Latin distringo - severe suffering) can complicate aspiration of gastric contents, DIC, infectious diseases of the lungs, especially pneumonia, various types of shock - septic, traumatic, posthemorrhagic, burn, as well as inhalation of toxic substances, including . excessive amounts of oxygen, paraquat, an overdose of drugs, heart surgery with extracorporeal circulation, and radiation exposure. More than 60% of patients with RDSV die, despite modern treatment methods. Mortality is especially high in the outcome of RDSV with aspiration of gastric contents (93.8%), sepsis (77.8%) and pneumonia (60%).

Pathogenesis and morphogenesis. RDSV is associated with damage to the endothelium of capillaries and often first-order pneumocytes in the area of ​​the airborne barrier with the subsequent development of respiratory failure. In the pathogenesis of early changes in RDSV, polymorphonuclear leukocytes play an important role. In experiments, it is possible to reduce damage to the lung tissue in neutropenia. The pathogenetic role of activated neutrophils is due to their generation of diverse factors:

1) proteolytic lysosomal enzymes;

2) free oxygen radicals;

3) nitric oxide;

4) derivatives of arachidonic acid (leukotrienes and prostaglandins) that activate phospholipase A;

5) platelet activation, leading to platelet aggregation and sequestration and production of platelet growth factor, which stimulates sclerosis processes.
Therefore, patients with RDSV often develop thrombocytopenia, and in the end - interstitial pulmonary fibrosis;

6) violations of the synthesis of surfactant by second-order pneumocytes, leading to the development of atelectasis.

In a number of conditions in the pathogenesis of RED, the generation of proteolytic enzymes, free oxygen radicals and nitrogen oxides not only by neutrophils, but also by alveolar macrophages and endothelium of alveolar capillaries (radiation, endotoxic shock, intoxication, etc.) comes first.

RDSV proceeds in three stages:

1. The preclinical stage is characterized by morphological signs of damage to the capillaries of the alveolar septa.

2. The acute stage is characterized by the development of interstitial and alveolar edema, it develops during the first week after the action of a damaging factor. At the same time, there are phenomena of intra-alveolar and interstitial edema, inflammatory changes with a large number of polymorphonuclear leukocytes and fibrin both in the intraalveolar exudate and in tissue infiltrates, hyaline membranes, atelectasis.

3. The stage of organization of exudate and proliferation of second-order pneumocytes ends with interstitial fibrosis. Organization processes begin on the 2nd – 3rd day of the disease.

Clinically, RDSV is characterized by the following manifestations: refractory hypoxemia, which cannot be corrected by increasing oxygenation of the respiratory mixture; decreased lung capacity; unchanged intracapillary and oncotic pressure; radiological symptoms of pulmonary edema. With the progression of RDES, interstitial pulmonary fibrosis develops. Death occurs from pulmonary heart failure.

Pulmonary hypertension. Pulmonary hypertension syndrome is characterized by increased pressure in the pulmonary circulation with the development of hypertrophy of the right ventricle, and subsequently of the pulmonary heart. Pulmonary hypertension syndrome can be primary and secondary.

Syndrome of primary pulmonary hypertension is extremely rare, as a rule, in children and women aged 20-40 years and has the morphology of plexogenic pulmonary arteriopathy.

The etiology of primary pulmonary hypertension has not been established. The literature describes family cases of the disease, inherited both in the dominant and recessive types. The disease also refers to polygenic pathologies, and the role of environmental factors is not excluded.

The pathogenesis of primary pulmonary hypertension syndrome is most likely autoimmune, as evidenced by the frequent development of plexogenic pulmonary arteriopathy in patients with proven autoimmune diseases (scleroderma, rheumatoid polyarteritis, goiter Hashimoto, primary biliary cirrhosis of the liver, etc.), as well as characteristic stenosis. arteries.

The role of hormones in the pathogenesis of plexogenic pulmonary arteriopathy is not ruled out, which is confirmed by the development of this disease in women of reproductive age, as well as during pregnancy and when taking oral contraceptives.

In the 70s. in Western Europe, cases of plexogenic pulmonary arteriopathy have been reported in women who used aminorex, in a chemical formula similar to epinephrine, to reduce weight.

Often, the diagnosis of primary pulmonary hypertension syndrome is made to patients with congenital malformations of the pulmonary artery and heart.

Morphological changes in the syndrome of primary pulmonary hypertension are characterized by the development of: atherosclerosis of the large branches of the pulmonary artery; fibrosis and muscle hypertrophy of the branches of the pulmonary artery of medium and small caliber.

Microscopic examination reveals a spectrum of changes corresponding to different stages of the progression of plexogenic pulmonary arteriopathy in the form of muscularization of the pulmonary artery, migration of dark muscle cells into intima, proliferation of intimal cells and transformation into myofibroblasts, the formation of plexogenic structures, dilatations (microaneurysms) and ruptures of microaneurysms, the development of fibrinoid .

Secondary pulmonary hypertension syndrome develops in chronic lung diseases, as well as in chronic left ventricular heart failure and repeated pulmonary thromboembolism. In the lungs, pneumosclerosis develops, and with stagnation of venous blood, pulmonary vasculitis and embolism, hemosiderosis joins.

In recent years, the development of pulmonary hypertension syndrome in chronic liver diseases, as well as chronic viral infections, has been of great interest.

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