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Alveolar Proteinosis

Alveolar proteinosis is caused by the accumulation of protein-lipoid substance in the alveoli. The histological picture is characterized by the presence in the lumen of the alveoli granular exudate with a CHIC-positive reaction. Transmitted by an autosomal recessive type.

Pathogenesis. A genetic defect that leads to the synthesis of a defective surfactant that does not have surface-active properties; This lipoprotein is characterized by a strong CHIC positive response; filling the alveoli with lipoprotein causes changes in lung function and the corresponding clinical symptoms: progressive shortness of breath, cough, chest pain, hemoptysis; further, the pulmonary heart is formed with the corresponding symptoms.

When X-ray diffraction, bilateral small-focal (small-point) darkening, which tend to merge, are determined, and fibrous changes are revealed in the future.

Biopsy: the presence of a CHIC-positive substance (confirmation of the diagnosis).

When electron microscopy detection in the alveoli and alveolar macrophages of surfactant in the form of lamellar bodies.

Treatment. Therapeutic bronchoalveolar lavage; purpose of trypsin, chymotrypsin.

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Alveolar Proteinosis

  1. Pulmonary alveolar proteinosis
    This is a rare disease, the cause and pathogenesis of which are unknown. Some patients have professional contact with various types of irritating (in particular, silicon) dust. On radiographs there is a diffuse darkening of the lung tissue. Macroscopically, in the non-falling lungs, massive dense areas are found, whitish-gray in the incision, emitting turbid liquid. Under
  2. Violation of alveolar ventilation
    Alveolar hypoventilation is a typical form of SVD disorders, in which minute alveolar ventilation (MAV) is less than the gas exchange requirement of the body. At the heart of the development of ventilation failure are 2 main mechanisms? a) violation of respiratory biomechanics (determined by pressure in the pleural cavity, alveoli, airways, gradients of these pressures, tracheobronchial
  3. Alveolar CO2 Voltage
    The alveolar voltage of carbon dioxide (РлСО2) reflects the balance between the total carbon dioxide production (production) (VCO2) and alveolar ventilation (CO2 elimination): PdCO2 = VCO2 / VA, where VA is alveolar ventilation (Fig. 22-21). RlCO2 depends much more on the elimination of carbon dioxide than on its production. Although in a stable state, the production and elimination of CO2 are equal, with acute
  4. Alveolar microlithiasis
    It is characterized by the formation in the pulmonary alveoli of the smallest stones, which consist of calcium carbonate and thiophosphates with a small admixture of iron salts and traces of magnesium. As a result of the deposition of calculus, an alveolar-capillary block occurs, the ventilation-perfusion relations are disturbed. Inherited by autosomal recessive type. Pathogenesis. Concretions in the alveoli
  5. Alveolar oxygen tension
    With each breath, the inhaled gas mixture is moistened in the upper respiratory tract at 37 ° C. Consequently, the partial pressure of oxygen in the respirable mixture (PiO2) is reduced due to the addition of water vapor. The saturated vapor pressure depends only on temperature and is equal to 47 mm Hg at 37 ° C. Art. In humid air at sea level, PiO2 is 149.3 mmHg. St.: (760-47) x 0.21 = 149, 3 mm
  6. Alveolar gopovtilyatsіya vnasldok porushennya activnost_ dikhalny m'yaz_v
    Tsya pathologia is zoomed by the nezdatnіstyu mezyazovogo aparata sterno klіtki heydznyuvati povnotsіnne dikhannya. Hypopathy is the main reason for retailing out of ailments with polyneuropathy, mysthenia, poliomacular, botulism, pravtsem, otrannymi phosphorus organisms. In diseases of the pathologic pathology, the poultice can be buried on the backslash of these relaxants in the early days
  7. Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.
    Pulmonary edema is cardiogenic and non-cardiogenic and is considered to be the immediate cause of death in every fourth deceased. Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7–9 mm Hg. st., it is slightly higher than that in the interstitium. The fluid is retained in the capillaries due to its viscous properties, rather high oncotic numbers.
  8. Mounier-Kun syndrome
    Clinical picture. From an early age cough with sputum, repeated exacerbations of bronchopulmonary disease, increase in respiratory failure during the period of exacerbation and with age. Deformation of the nail phalanxes in the form of "drum sticks". Radiographic signs: deformation of the pulmonary pattern with areas of consolidation. The expansion of the lumen of the trachea and large bronchi. Bronchiectasis in the inferior
  9. Typical disorders of gas exchange lung function.
    Are the following typical violations of gas exchange lung function? 1. Violation of alveolar ventilation? a) alveolar hypoventilation b) alveolar hyperventilation c) uneven ventilation 2. Disturbance of lung perfusion. 3. Violation of ventilation and perfusion relationships. 4. Violation of diffusion capacity of the lungs. Mixed
  10. Idiopathic fibrosing alveolitis.
    Idiopathic fibrosing alveolitis (ELISA) is not a single nosology. It is believed that currently ELISA is a group of diseases that includes the following units: classical interstitial pneumonia, "nonspecific" interstitial pneumonia, desquamative pneumonia, bronchiolitis obliterans with organized pneumonia, and giant cell interstitial pneumonia. Early
  11. Voltage of carbon dioxide in the blood of the terminal pulmonary capillaries
    Fig. 22-21. Effect of alveolar ventilation on alveolar PCO2 at two rates of formation of CO2. (With permission. From: Nunn JF Applied Respiratory Physiology, 3rd ed. Butterworths, 1987.) The voltage of CO2 in the blood of the terminal pulmonary capillaries (Pc'CO2) is almost identical to РлСО2, which is due to the same reasons as for {foto48} oxygen. In addition, we indicate that the rate of diffusion of CO2
  12. Carbon dioxide tension in the final portion of the exhaled gas
    The final portion of the exhaled gas is practically an alveolar gas, and РлСО2 is practically identical to PaCO2, therefore the CO2 voltage in the final portion of the exhaled gas, РктСО2, is used clinically to evaluate PaCO2 (Chapter 6). The difference between РлСО2 and РктСО2 normally does not exceed 5 mm Hg. Art. and due to dilution of alveolar gas by gas from non-perfused alveoli that do not contain CO2 (t.
  13. Restrictive lung diseases
    Causes of restrictive lung disease Causes of acute restrictive disease: • ????? pulmonary edema; • ???? ARDS; •????aspiration; • ???? neurogenic edema; • ????? opioid overdose; • ???? congestive myocardial insufficiency; • ???? pleural effusion; •????pneumothorax; • ???? increase mediastinum; • ???? pneumomediastinum. Chronic lung disease leading to restrictive
  14. Bronchoalveolar lavage
    This intervention is performed with pulmonary alveolar proteinosis, which is characterized by excessive synthesis of surfactant and the impossibility of its effective clearance. The disease is manifested by shortness of breath, on the chest radiograph, bilateral darkening is visible. Bronchoalveolar lavage is indicated for severe hypoxemia or in the case of progression of shortness of breath. Simultaneously perform lavage only
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