It is for cholesterol deposition, holesterinovite esters and neutral fat in the arteries of the intimate. Etc. are formed atherosclerotic plaques, which have three main components:
A. cellular composition - mainly smooth muscle, macrophages and T - lymphocytes
2. extracellular matrix including collagen, elastic fibers, proteoglycans and
3. intra-and extracellularly deposited lipids, cholesterol crystals
These components are found in different proportions and configurations for different lesions. Most often the surface of plaques in the aorta ateromatoznite visible fibrous layer ("top") composed of smooth muscle cells and relatively dense collagen. Below it is the necrotic core of plaque, etc.. etc. athera, containing lipids, cholesterol and cholesterol esters, detritus from dead cells and foam cells. In the periphery of the lesion is an area of neovascularisation, proliferation of small blood vessels. In advanced atherosclerotic plaques are found in calcifications. On histological preparation of the aorta is seen splitting cadovata wall between intimate and media blanks and optical processing of soluble holesterinovite crystals and lipids

Demonstration of lipids in hepatocytes is implemented using kriostatni cuts only on fresh or fixed in formalin material, but not on vlklyucheni histologically in paraffin processed tissue fragments. Thus, the material does not pass into alcoholic solutions, lipids do not dissolve and can be colored with lipoboi. The most commonly used method is coloring Sudan III, where the lipids are visualized as orange-drops in the cytoplasm of hepatocytes

Fatty liver, also known as fatty liver disease (FLD), is a reversible condition wherein large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis (i.e., abnormal retention of lipids within a cell). Despite having multiple causes, fatty liver can be considered a single disease that occurs worldwide in those with excessive alcohol intake and the obese (with or without effects of insulin resistance). The condition is also associated with other diseases that influence fat metabolism.^[1]It is difficult to distinguish alcoholic FLD from nonalcoholic FLD, and both show microvesicular and macrovesicular fatty changes at different stages.
Accumulation of fat may also be accompanied by a progressive inflammation of the liver (hepatitis), called steatohepatitis. By considering the contribution by alcohol, fatty liver may be termed alcoholic steatosis or nonalcoholic fatty liver disease (NAFLD), and the more severe forms as alcoholic steatohepatitis (part of alcoholic liver disease) and Non-alcoholic steatohepatitis (NASH).

1-Necrosis renis /№ 34. Infarctus anaemicus renis/.
Anemic infarction of the kidney develops in blockage of some of the branches of renal areteriya - obiknovino of embolism, resulting in ischemia occurs with subsequent necrosis of the renal parenchyma in the relevant section. It is a coagulation necrosis, presented in a section of the body with preserved structure in which the visible shadows of glomeruli and tubules. In cells lacking nuclei tubes and homogenized cytoplasm, intense pink colored XE. Disappear cellular details can be seen only vaguely delineated cell borders. Morphological features of necrosis are different phases of nuclear fission: homogenization (compaction) of the nuclear chromatin - karyopycnosis, degradation of nuclei presented in the form of pellets - karyorrhexis and complete disappearance in necrotic cells - karyolysis. Affected cell and tissue structures are homogenized granular cytoplasm and stained more intensely than eozina. Around the area of necrosis is hiperemichnohemoragichnata area consisting of dilated blood vessels and bleeding. Near it there is segmented shaft of leukocytes, which may be missing in early stages. Adjacent renal tissue is found with a fully preserved structure.

 2. Necrosis pulmonis /№ 58 Bronchopneumonia tbc caseosa./
Kazeozna necrosis of the lung is most commonly seen in kazeozna bronchopneumonia or in the center of granulomas formed in tuberculosis. It is represented by nonstructural, drebnozarnisti areas completely deleted sinkavorozov alveolar structure and color of stain H & E. Among the nonstructural fields can be monitored and blue colored remnants of nuclear chromatin resulting from karyorrhexis. Around the necrotic zone are macrophages, monocytes that migrated from the blood flow in relation to the cellular response to chronic irritation. They are formed epiteloidni cells with oval nuclei and pale pink cytoplasm. With its form and arrangement they resemble epithelial cells, where labeled cells si.Sred epiteloidnite meet multicore type giant cells "Langhans" resulting from the merger of several epiteloidni cells. Their nuclei are located along the periphery of the cell in the form of a horseshoe with an opening to the central necrosis of the periphery of the granuloma are described T lymphocytes forming etc. lymphocyte shaft.

3. Necrosis lymphonodi. (=№58 Tuberculosis lymphonodi)
The process is represented by a centrally located area of necrosis in kazeozna lymph node - a large, structureless, rose-colored mass, which one can see the blue colored drebnozarnisti fragments of nuclear chromatin. About kazeoznata necrosis are characteristic features of spindle cell epiteloidni ordered palisades / boards as a fence /. Among them are found Multinucleated giant cell type "Langhans. Under the fibrous capsule of the lymph node on the periphery of the necrotic area is visible reserved lymph follicles.

4. Necrosis myocardii /=№35 Infarctus anaemicus myocardii).
This study demonstrates the preparation ischemic / anemic / coagulation necrosis in the myocardium as a result of stopping the blood flow, due mostly to the blockage of coronary artery by a clot or prolonged vasoconstriction. In anemic / white / myocardial infarction was observed well homogenized limited area of cardiomyocytes, which have lost their transverse nabrazdenost and stained more intensely than eozina. Nuclei are not clearly visible. Among the necrotic cardiomyocytes reserved visible elements of the interstitial connective tissue and blood vessels from the shadows. After 6 to 8 hours of initial clinical manifestation of myocardial necrotic fields are separate from the surrounding tissue through etc. hyperemic-hemorrhagic area represented by dilated blood vessels and bleeding, and later by inflammatory leukocytes segmented shaft