49. Chronic general venous plethora: definition, causes, pathogenesis. Pathological changes in organs, outcomes, clinical significance.

Chronic general venous fullness develops in the syndrome of chronic cardiac (cardiovascular) or pulmonary heart failure.

Its causes are heart defects, chronic ischemic disease, chronic myocarditis, cardiomyopathy, pulmonary emphysema, pneumosclerosis of various origins (cirrhotic forms of pulmonary tuberculosis, chronic pneumonia, pneumoconiosis), curvature of the spine (scoliosis, kyphosis, lordosis), overgrowth or obliteration of pleural cavities with adhesions in pleurisy, etc.

Pathogenesis: By maintaining the state of tissue hypoxia for a long time, it determines not only plasmorrhage, edema, stasis and hemorrhages, dystrophy and necrosis, but also atrophy and sclerosis. Sclerosis is associated with chronic hypoxia, which stimulates collagen synthesis by fibroblasts and fibroblast-like cells. Connective tissue displaces parenchymal elements, and stagnant compaction (induration) of organs and tissues develops. The vicious circle in chronic venous fullness is closed by the development of capillary parenchymal block due to thickening of the basement membranes of the endothelium and epithelium due to increased collagen production by fibroblasts, smooth muscle cells and lipofibroblasts.

Morphogenesis of changes in the liver:

The liver is Macro-enlarged, dense, the edges are rounded, the incision surface is mottled, gray-yellow with dark red speckles, resembles nutmeg (brown induration of the liver). Micro-: the central parts of the lobules are full-blooded, hepatocytes are destroyed, on the periphery hepatocytes are in a state of fatty degeneration.

Morphogenesis of changes in the lungs: Macro-: enlarged, dense, brown (brown lung induration). Micro-: multiple diapedetic hemorrhages, hemosiderosis, sclerosis.

The outcomes of venous fullness of the lungs and liver: pneumosclerosis of the lungs, DN and cirrhosis of the liver, liver failure.

50. Brown induration of the lungs: definition of the concept, causes, pathogenesis. Macro- and microscopic changes in the lungs, outcomes, clinical significance.

Brown lung induration is a diffuse overgrowth of connective tissue in the lung with focal deposits of iron-containing brown pigment and an abundance of hemosiderophages, developing as a result of prolonged stagnant fullness of the small circulatory circle, e.g. in rheumatic heart defects.

The main causes of the development of brown lung induration.Chronic general venous fullness develops in chronic cardiovascular insufficiency syndrome, which complicates many heart diseases:

• coronary heart disease;

• congenital and acquired heart defects;

• hypertension and symptomatic arterial hypertension;

• myocarditis, etc.

Morphogenesis of brown lung induration

• Chronic venous fullness and hypertension in the small circle of blood circulation.

• Adaptive reconstruction of pulmonary veins and arteries.

Micro-: Clusters of hemosiderin–loaded cells - sideroblasts and siderophages and free-lying hemosiderin appear in the alveoli, bronchi, interalveolar septa, peribronchial connective tissue, lymphatic vessels and lung nodes. Diffuse hemosiderosis of the lungs occurs. Hemosiderin turns brown when stained with hematoxylin and eosin.

Macro-: The lungs are enlarged in size, dense consistency, on the incision in the lung tissue — multiple small inclusions of brown hemosiderin, layers of connective tissue in the form of a diffuse gray mesh, overgrowth of connective tissue around the bronchi and blood vessels (chronic venous fullness, local hemosiderosis and lung sclerosis); pulmonary edema is pronounced — an abundance of foamy light liquids on the incision surface.

Outcome: Pneumosclerosis and hemosiderosis with brown lung densification have a caudoapical distribution and depend on the degree and duration of venous congestion in the lungs.

Clinical significance:

Violation of gas exchange and other lung functions;

In patients with brown lung induration, sputum has a rusty color due to the formation of "heart defect cells" (hemosiderin-loaded siderophages). The detection of "heart defect cells" is of diagnostic importance for determining decompensation in heart defects.