155. Bronchiectasis: definition, classification, pathogenesis, morphogenesis, pathological anatomy, complications, clinical significance.

Bronchiectatic disease (Bronchoestasis) is a disease characterized by irreversible expansion of the bronchi and bronchioles (bronchiectasis) due to the destruction of their smooth muscle tissue and elastic framework against the background of chronic necrotizing infection. Classification 1. By the time of occurrence - Congenital (obr cystic lung) - Acquired (due to chronic bronchitis) 2. By the mechanism of occurrence - Destructive - viral - bacterial infections - Obstructive - Atelectatic - Sclerotic 3. In shape - Cylindrical - Baggy - Mixed 4. By nature - Serous - Purulent

Pathogenesis: obstruction and infection – impaired clearance – accumulation of secretions – inflammation of the respiratory tract distal to the obstruction – necrosis – dystrophy – sclerosis.

Morphology: occur in the lower lobes of both lungs – the airways are dilated. Cysts with mucopurulent contents and abscesses may form. Pseudostratification and squamous cell metaplasia of the epithelium.

Clinic: severe cough with hemorrhagic sputum, shortness of breath, cyanosis.

Complications: 1) abscesses, 2)fibrosis, 3) hypertension in the small circle of blood circulation and ventricular hypertrophy (pulmonary heart), 4) amyloidosis

156. Pulmonary emphysema: definition, types, mechanisms of development, pathological anatomy, outcomes, complications, clinical significance.

Emphysema of the lungs is an excessive air content in the lungs and an increase in their size.

Classification: centroacinar (the central part of the acinus is affected), panacinar (damage to the entire acinus), paraseptal (the periphery of the acinus is affected), irregular (lesions near the scars).

Pathological anatomy. The lungs are enlarged, cover the anterior mediastinum with their edges, swollen, pale, soft, do not fall off, crunch appears when cut. Mucopurulent exudate is separated from the lumen of the bronchi, the walls of which are thickened, when pressed. The mucous membrane of the bronchi is full-blooded, with inflammatory infiltration, a large number of goblet cells. The muscle layer is unevenly hypertrophied, especially in the small bronchi.

Pathogenesis. The destruction of the elastic membranes of the alveolar wall is based on the protease-antiprotease mechanism, due to an oxidant-antioxidant imbalance. There may be a congenital defect of alpha-1 antitrypsin (antiprotease) and acquired due to increased activity of leukocytes and macrophages in chronic bronchitis caused by the action of cigarette smoke and infections. Proteases destroy the elastic framework of the interalveolar septa.

Morphology: increased lung volume; bull formation (blisters); enlarged and thickened pores of the Cone (holes in the interalveolar septa);

Clinic: 1) cough; 2) loss of body weight; 3) barrel chest and shortness of breath with a clear prolongation of exhalation time (the patient usually sits bent over and breathes through compressed lips).

Complications: 1) pulmonary heart; 2) respiratory acidosis and coma; 3) right ventricular failure; 4) massive collapse of the lungs as a result of secondary pneumothorax.