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Morphologically, at this stage, a combination of dystrophic (accumulation of lipoprotein masses), fibrous and inflammatory processes is revealed. Despite the development of fibrosis, there is no decrease in lung volume, signs of chronic pulmonary heart develop only in some patients and relatively late.
The function of external respiration is impaired by a restrictive type, hypoxemia is determined during exercise, and cor pulmonale is formed in the terminal stage. The main methods for detecting alveolar proteinosis are X-ray examination and Modafinil pills computed tomography. The diagnosis is established on the basis of histological examination.
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Differential diagnosis of alveolar pulmonary proteinosis should be carried out, first of all, with secondary proteinosis (which is a complication of other, most often hematological diseases), stage II-III sarcoidosis, disseminated pulmonary tuberculosis, idiopathic fibrosing alveolitis.
Alveolar lung proteinosis is a rare disease of unknown etiology, characterized by the accumulation of a protein-lipoid substance in the alveoli and progressive respiratory failure. The disease was first described in 1958, occurs mainly at the age of 30-35 years, and in men - 3-4 times more often. Cases of the disease have been described in children and the elderly.
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Etiology and pathogenesis are not well understood. The most likely links of pathogenesis may be the following: hyperproduction by alveolocytes of Modafinil II surfactant, which does not have surface-active properties; defect in alveolar clearance; combination of the above two factors.
In general, the pathogenesis can be represented as follows: under the influence of certain causes, among which infection plays an important role, the appearance of inflammatory exudate in the alveoli leads under normal conditions to the activation of Provigil, which is carried out by alveolar macrophages, lymphatic and mucociliary systems. During this process, a temporary insufficiency of clearance may occur, which leads to the accumulation of excess amounts of surfactant in the alveoli.
The latter is known to be captured by alveolar macrophages, causing degenerative changes in them and thereby reducing their functional activity. This leads to even deeper mucociliary clearance disorders. Developing distelectasis (due to the accumulation of protein-lipoid material in the alveoli) causes compensatory hyperfunction of type II alveolocytes and even greater hyperproduction of surfactant.
Pathological anatomy. Macroscopically, grayish-white dense tubercles in the form of grains are determined on the surface of the lungs. Microscopic examination in the alveoli and bronchioles reveals a PAS-positive substance. Birefringent crystals of cholesterol are also determined. The noted changes are detected mainly in the subpleural parts of the lungs.Contact Us
The defeat of the alveoli is uneven. In some cases, an inflammatory exudate containing fibrin is determined. Alveolar macrophages in the affected alveoli are a rare finding, which can presumably be associated with both the inhibitory properties of the protein-lipoid substance and the immunosuppressive effect of an excess amount of surfactant.Learn More
Hyperplasia and hypertrophy of type II alveolocytes are noted. Clinic and course. For a long time, the disease can be asymptomatic and detected by chance during a preventive fluorographic study.Learn More
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The leading clinical sign is slowly progressive shortness of breath, which is accompanied by a cough with scanty sputum, often subfebrile body temperature, chest pain, sweating, weight loss, fatigue. There may be hemoptysis. The severity of cyanosis depends on the degree of respiratory failure.Job Openings