Autopsy results

A macroscopic examination revealed pulmonary edema. Marked adhesions of the interlobar pleura, parietal and visceral pleura. A fluid (transudate) was found in both pleural cavities. The lung tissue to the touch was a testy consistency, differed by its low airiness, had a net-like pattern on the cut. Histological examination of the lungs revealed lymphoid and plasma cell infiltration in the form of cords in the interalveolar septa, along the vascular adventitia, in the submucosal bronchi and in the peribronchial spaces, manifestations of pulmonary paraproteinosis (the protein masses filling the pulmonary alveoli created carnivorous spaces. lungs impregnated thickened, hyalinized interalveolar partitions and filled small vessels), pneumosclerosis,the presence of uremic lesions – pneumonitis (small focal nature of the lesion, extending to 5-20 alveoli, the presence of one and the same the source of circulatory disorders , edema and fibrinous inflammation), calcification. The thickness of the diaphragm is 3.9 mm. Medium sized myocytes prevailed. But an increase in large and small sized myocytes was noted (15 and 38%, respectively). There was a significant growth of the stroma around the vessels, in the intermuscular space (28%) and large areas of lipomatosis. Revealed protein stasis in small vessels of the diaphragm.

The data of regional ventilation and blood flow were analyzed and compared with morphological changes in the lungs in patients with MM. In patients with group II (stage IIIIA), paraproteinosis of the lungs and amyloidosis, lymphoid and plasma cell infiltration of the lungs and bronchi, pneumosclerosis, localized compensatory emphysema, microcirculation disorders and diaphragm function were diagnosed. The leading factor contributing to the development of microcirculatory disorders in this group is the plasma hyperhazard. Due to the pathology of the microvasculature, tissue trophicity is disturbed, local metabolism suffers, and tissue hypoxia develops. Thinning occurs, sclerosis of the bronchial mucosa. In 40% of patients with MM, bilateral diffuse atrophic endobronchitis develops.Against this background, due to immunodeficiency, bronchopulmonary infections acquire a severe and prolonged course. In case of myelomatosis of the diaphragm and violation of the chest excursion, the mobility of the primary respiratory muscle decreases. These pathological changes explain the decrease in general and regional ventilation, pulmonary blood flow in patients with MM.

In group III (with the addition of renal failure) in the lungs and bronchi, manifestations of nephrogenic edema, uremic pneumonitis and calcinosis are revealed, microhemocirculation and hemodynamic disorders of the ICC are progressing, which further aggravates the pulmonary ventilation.

The presence of specific myelomatous and uremic changes in the lungs, severe and prolonged course of bronchopulmonary infections, impaired lung ventilation function and bronchial drainage function, impaired chest excursion due to destruction of the ribs and spine lead to the development and progression of hypoxemia. In patients with MM in stage IIIA and with accession of chronic renal failure, endothelial dysfunction occurs . Patients with renal insufficiency develop acidosis. Hypoxemia, endothelial dysfunction, myocardial dystrophy and acidosis contribute to an increase in pressure in the pulmonary artery system with MM.

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