39. Hemorrhagic infarction: definition, causes, localization. Macro- and microscopic changes in organs, outcomes. Clinical significance.

In case of a red (hemorrhagic) infarction, the area of necrosis is soaked in blood, it is dark red and well delimited. A favorable condition for such hemorrhagic impregnation is venous stagnation . Hemorrhagic infarction occurs, as a rule, in the lungs, intestines, rarely in the spleen, kidneys.

A red (hemorrhagic) infarction is characterized by the fact that the area of necrosis is soaked in blood, it is dark red and well delimited. The infarction turns red due to the release of blood from necrotic vessels of the microcirculatory bed in the infarction zone. For the development of a red infarction, the features of the angioarchitectonics of the organ are important – two or more blood flow systems, the development of collaterals: in the lungs – the presence of anastomoses between the bronchial and pulmonary arteries, in the intestine – an abundance of anastomoses between the branches of the mesenteric arteries, in the brain in the area of the Willis circle anastomoses between the internal carotid and branches of the basilar arteries. Red infarcts can also occur in the tissue when the obstructing thrombus dissolves or fragments (disintegrates), which resumes arterial blood flow in the infarction zone.

40. Apoptosis: definition, causes, pathogenesis - biochemical and microscopic features.

Apoptosis is a type of programmed cell death that occurs due to the sequential activation of "death genes" and enzymes of the "suicidal biochemical pathway". Cell death occurs with the participation of protein products of certain genes, although in some cases similar morphological changes can be obtained without gene activation.

The biological meaning of apoptosis is the elimination of damaged cells and, being in a dynamic balance between the processes of cell proliferation and differentiation, the ability to maintain tissue homeostasis at a certain level.

The peculiarity of apoptosis is that apoptosis does not cause inflammation in the surrounding tissues. The reason is the preservation of the membrane and → isolation of damaging cytoplasmic factors until the complete completion of the process (O2- , H2O2, lysosomal enzymes). This feature is an important positive feature of apoptosis, unlike necrosis. In case of necrosis, the membrane is damaged (or ruptured) immediately. Therefore, during necrosis, the contents of the cytoplasm are released (O2- , H2O2, lysosomal enzymes). There is damage to neighboring cells and an inflammatory process. An important feature of apoptosis is the removal of dying cells without the development of inflammation.

Reasons: The apoptosis program can be started either as a result of the receipt of a cell death signal, or when the supply of survival factors stops. An example of a signal for apoptosis may be the binding of tumor necrosis factor (TNF) to the corresponding receptor located on the surface of lymphocytes. The cessation of the supply of hormones or growth factors necessary for the survival of certain cells becomes a "negative" signal for apoptosis. Thus, a decrease in the concentration of testosterone in the blood after castration is accompanied by apoptosis of prostate cells.

The pathogenesis of apoptosis includes biochemical and genetic mechanisms of its regulation:

• Cleavage of proteins by cysteine proteases (caspases).

• Crosslinking of proteins by transglutaminases into a single connected network and dehydration of cells due to the action of special selective enzyme transport systems regulating the exchange of potassium, sodium, chlorine and water ions.

• The destruction of the nucleus by calcium/magnesium-dependent endonuclease, which cleaves DNA molecules in the areas between nucleosomes, which leads to the formation of DNA fragments of the same size. The peculiar cleavage of DNA during apoptosis has its own morphological expression in the form of a special chromatin structure.

• Damage to the structure of the cell membrane, accompanied by the movement of phosphatidylserine from the inner to the outer surface of the cytolemma. A change in the biochemical organization of the cytolemma during apoptosis is crucial in the recognition and immediate phagocytosis of apoptose bodies by neighboring cells, which prevents the ingress of various biologically active substances into the environment and thereby prevents inflammatory and other pathological reactions.