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

5. Necrosis cerebri /=№ 36. Infarctus anaemicus cerebri – encephalomalacia.
It is for anemic infarction due to obturation of the thrombus or thromboembolism artery in the brain. Necrosis is kolikvatsionen type, characteristic of cells and tissues poor in protein and rich in water and lipids. When hypoxia occurs the death of brain cells, which is manifested by "softening" of brain matter, etc. encephalomalacia. Microscopy in the area of necrosis is seen stretch of pale pink colored, homogeneous, structureless granular matter with a view or as a single thread veins. Gangliyni and glial cells, and nevrofibrili not observed. On the border with preserved tissue are very large cells with bright nuclei and sometimes piknotichni swollen, vacuolated cytoplasm, which detect lipids and brown pigment / hemosiderin. The same is formed by the disintegration of erythrocytes in the hearth of necrosis and their phagocytic glial cells. These cells are ingested and dissolved lipids of myelin sheath. They are marked as lipofagi (psevdoksantomni cells) and cells derived from mikrogliyata. When staining for lipids in Sudan III kriostatni cuts on their cytoplasm are stained yellow-orange. If fatalities occur after receiving the attack (stroke), the process of necrosis ends with the formation of glial scar formation or a pseudocyst. Years later when an autopsy can be found psevdokistata attesting spent cerebral infarction.

6. Emphysema pulmonis. Pulmonary emphysema is a process of destruction and dilation of the airways distal to terminal bronchioles. In the most common form - panatsinaren histological picture of emphysema in the lung is represented by: - Advanced respiratory bronchioles, alveolar moves alveoli and pores of Cohn. - Destroyed mezhdualveolarni baffle. - Thin alveolar walls, poor in elastic fibers. - Reduced number and poor alveolar capillary wedge kravonapalneni. - In the alveoli and alveolar interstitial macrophages are loaded with pigment antrakotichen / koniofagi /.

7. Atrophia fusca hepatis.
Brown atrophy of the liver is observed in the course of diseases associated with failure and inferiority of nutrition: idiopathic pyloric stenosis or gastric / doudenalna ulcer, cancer of the stomach and esophagus, cachexia, incl. and senile, diseases of the endocrine glands etc.. Macroscopically, the liver is reduced in size to brownish, thickened and sharp edge. Histological picture is represented by thin gredichki liver, mainly in centrilobular areas. Delchetata are reduced in size and portal spaces appear dilated. Hepatocytes around v. centralis are reduced in size (atrophic) in the cytoplasm, perinuklearno, there is accumulation of yellow-brown pigment - lipofuscin.

8. Cell swelling / Dystrophia parenchymatosa renis /
Home of the cell damage due to most of the effects of hypoxia, toxic or infectious factors. It is for intracellular edema. The process is reversible upon removal of etiopatogenetichniya factor. With persistence, the impact goes into a severe severe cellular or tissue damage, incl. and necrosis. Most often this process occurs in the epithelial cells of proximal convoluted tubule of the kidney. The boundaries between cells are not well visible. Ducts are enlarged, and their lumens are irregular because they prominirane of swollen epithelial cells that stained intensely for XE are colored pink. In the process progresses in the cytoplasm may form vacuoles representing dilated cisterns of endoplazmatichniya reticulum. Hence the name or vakuolerna hidropichna dystrophy - a more advanced stage of intracellular edema.

9.Corpus albicans ovarii. It is a physiological delay in involyuiralite yellow hyaline bodies in the fibrous stroma of the ovary. Because macroscopic deposition of hyaline in them they become white, and where bear its name. White bodies are final phase in the evolution of the Graafian follicle. Under the microscope appear as homogeneous pink-colored eozina of nonstructural forms. Their bodies are well-demarcated from the surrounding tissue folded in the form of swag border, tend to lobubirane

№ 10. Fibrinoidna necrosis (bottom of a stomach ulcer).
The product is an example of local deposition of fibrinoid necrosis in the mucous membranes in the case at the bottom of chronic stomach ulcer. The
Проксимални тубули
гломерули process is referred to as fibrinoidna necrosis and is a sign of exacerbation of the ulcer. Pathological findings is the result of changes in collagen fibers under the influence of end-of-vessels plazmenni protein albumin, globulin and fibrinogen. In this process, receive solid, insoluble compounds, stained pink from eozina who perished together with local cells form a layer fibrinoidnata necrosis. There remain four areas of the plague - surface, consisting of cellular detritus and inflammatory exudate of segmented leukocytes, fibrinoidna necrosis zone, represented by pink and blue uniform stripe layer of granulation tissue which is located in a mature fibrous tissue.

The process is subendotelno hyaline deposition in the walls of arterioles as a result most of arterial hypertension. In preparation is presented in the deposition of hyaline walls of small arteries and arterioles of the kidneys. Vascular walls are unevenly thickened, homogeneously pink colored HE. Depending on the severity of their lumens process with varying degrees of narrowing. The worst injured were the walls of glomeruli privodyashtite vessels - arterioles in their vascular pole (vasa afferens), which can be seen in cross-section as pink rings.

12. Amyloidosis renis (HE).
Amyloid appears as a homogeneous, pink colored by eozina, structureless substance in renal structures. Glomeruli are affected to varying degrees - from the homogenization of individual capillaries in the early stage, to cover all the glomeruli of the process. Damaged glomeruli are larger than normal as a result of their accumulation of abnormal protein. Shows the preparation and accumulation of pink colored protein in the walls of vessels of medium and small caliber and in the basal membrane of the seminiferous that are thickened. The process leads to fatty degeneration in epithelial cells them due to chronic hypoxia associated with reduction in glomerular blood flow. Fatty degeneration of the epithelial cells of proximal tubules is the cause of macroscopic findings "ren albus".

13. Amyloidosis renis (MV).
In preparation for staining with metilviolet property is used to amyloid metahromatichno colors of some aniline dyes. The process is called metahromaziya violet paint colors metilviolet amyloid selectively in red and other tissues retain its main blue-violet color. Histologically all structures, with enlarged size of the amyloid deposits are stained red. / Parts or whole glomeruli glomeruli, vessel walls and basement membrane of ducts /.

14. Amyloidosis lienis (HE).
Deposition of amyloid in the spleen may be focal in the form of homogeneous pink-colored lymph follicles with eozin / t.n.sagova spleen / or as diffuse deposits in the walls of the sine wave and connective network of the red pulp / Ham-derson spleen /. The name derives from the spleen Sagova its macroscopic appearance - when she cut dotted with small whitish nodules, like grains of sago. In preparation demonstrate hearth deposition in follicles that are enlarged. Centrally located follicular arteries affected by the process are also homogenized, thickened with pink colored walls.

15. Amyloidosis lienis (MV).
Stained with metilviolet deposits in lymph follicles and their central arteries amyloid is red, and other tissues are blue-violet. This method is used for proof of amyloidosis in differential diagnosis with other processes.

16.Carcinoma gelatinosum (HE).
The presented case is a demonstration of glandular cancer / adenocarcinoma / intracellular and extracellular sluzoobrazuvane. In the malignant transformation of glandular cells due to impaired metabolism of glikoproteidite they occur nekotroliruema production of mucus. In the early form intracellular mucus vacuoles. Later they merged to form a mucus drop, forcing the core to the periphery of the cell. It begins to look like a "ring with a stone." Thoroughly congested with mucus cells die and form lakes of mucus, dyeing basophilic - in sinkavovioletov color. Among them. visible single cell type "ring with a stone."

17.Carcinoma gelatinosum (alcian blau ).
Glikoproteidite are complex organic compounds of proteins with polymerized hydrocarbons. Depending on their location, in violation of their metabolism accumulate neutral or acidic mucopolysaccharides. An example is again zhelatinozniyat, mucus producing adenocarcinoma. Preparation indicates the presence of acid mucopolysaccharides in tumor cells and lakes of mucus around them has been used to color blue altsianovo their demonstration. Histologically visible blue-green mucus sections and single cancer cells with blue stained mucus droplets

18. Mucoviscidosis pancreatis. Cystic Fibrosis / cystic fibrosis / a hereditary disorder of epithelial transport of chloride ions in mucus secretion in exocrine glands and the lining of the respiratory, gastrointestinal tract and pancreas In this case, the process affects pancreatic ductal cells from which the component produced exceptionally phlegm, blocked outgoing channels of the gland. They are expanding due to fluid retention with subsequent formation of retention cysts. The process is coupled with glandular atrophy and fibrosis around the canals. The preparation is described seeing changes - mostly dilated ducts filled with mucus retention periduktalnata fibrosis and cysts containing mucus pink homogeneous material.

19. Nаevus pigmentosus.
Pigment nevus is congenital or acquired benign neoplasm originating from dendritic melanocytes localized in the basal layer of epidermis. In this case it is seen as an example of impaired metabolism of aboriginal pigment melanin produced by dendritic melanocytes. Nevus can occur in various forms but the most common are: border, dermal, complex, spitz nevus, and nevus dizplastichen. In this case demonstrates dermal nevus. In melanocytes proliferate as it shaped nests in the epidermis. Usually they contain brown granules of melanin, the pigment but may not be evident. The nests are composed of uniform round or polygonal cells drained, with homogeneous or slightly granular cytoplasm and large round or oval nucleus. Nevus can give early malignant pigmented tumors - malignant melanoma.

20. Induratio fusca pulmonis (HE)
The process demonstrates the local deposition of haemosiderin in the lungs in chronic left heart failure (especially in congenital or acquired in later defects of the mitral valve). As a result of chronic venous stasis in the alveolar capillary wedge there is hypoxia, which leads to damage of endothelial cells and their permeability to increase. By diapedeza erythrocytes appear in the lumen of the alveoli, where phagocytosed by macrophages located there, in this case denoted as hemosiderofagi. In their hemoglobin is converted into ferritin, which aggregates in zlatistokafenikavite hemosiderin granules. Meanwhile, hypoxia leads to proliferation of fibroblasts to produce collagen and thickening of the
епидермис alveolar walls. In the alveoli and the interstitial are many hemosiderofagi. Hemosiderofagite can be found in the sputum of patients as a diagnostic test and therefore are called cells of the heart defect (Hertzfehlercellen)

21.Induratio fusca pulmonis (Histochemical reaction to demonstrate the Fe + + in the structure of hemosiderin).
To prove the nature of the postponed in brown induration of lung pigment / hemosiderin / used histohimichnata Max Perls reaction and with ferotsiankalii tsolna kitselina etc. Berlin blue. Hemosiderinat turns sinkavozeleno. Histologically observed glaucous granules in the cytoplasm of siderofagite located in the lumen of the alveoli.

22.Icterus renis. With increased level of bilirubin was observed in the deposition of the seminiferous epithelium, Henle's loop and more rarely in these legal and collecting tubules of the kidney. In the affected cells are found small greenish-brown grains. In the later stage these cells in the lumen of husked and ducts with bile acids and bile salts form cylinders. The epithelial cells of the proximal part of nephron develop dystrophic and necrotic changes, which represent the morphological equivalent etc. hepato-renal syndrome.

23.Anthracosis pulmonis The product is an example of exogenous pigment deposition in the lung - coal dust. Inhaled dust particles smaller than 5 microns mukotsiliarnata overcome the barrier of traheobronhialnoto tree and reach the alveoli where phagocytosed by alveolar macrophages. Phagocytosed dust particles, they are called macrophages koniofagi and the process is referred to as antrakoza. Histologically visible koniofagi whose cytoplasm contained black powder inclusions. After the death of koniofagite antrakotichniyat pigment is deposited in the interstitial connective tissue - in the walls of the alveoli, in the course of Sep subplevrano, peri-bronchially.

24. Steatosis hepatis = Dystrophia adiposa hepatis (HE).
Otlaganeto at lipidi under the format trigliceridi in černiâ CE nablûdava when fraction uvreždaniâ toksični hipoksični s″stoâniâ, zaharen, diabetes, zatl″stâvane, etc. and CE označava Kato steatoza. Kasai Xie nay-frequently for natrupvaneto in hepatocitite under the format kapčici, koito when ocvetâvane with hemalaun eozin se viždat Kato optically prazni vacuoles, t″j Kato with his SA ekstrahirani parafinovata processing of alkohola. In zavisimost from goleminata, Breu and razprostranenieto in hepatocitite černodrobnata steatoza se podrazdelâ to ogniŝna and difuzna, drebnokapčesta and edrokapčesta. Histologično strukturata to černiâ fraction (e) well. In the portalnite space hepatocitite zonite about fatty vacuoles and s″d″ržat tezi at centralnite at delčetata near centralnite CA Veni a comparatively s″hraneni. Zonalnoto otlagane to mazninite dependence of proces″t, kojto go e predizvikal. When hipoksiâ obiknoveno SA zasegnati centrolobularnite zone, toksični v″zdejstviâ, buying uvreždaŝiât on the kr″vniâ current agent idva e steatozata periportalnite zone at delčetata. Obilnoto natrupvane to dovede to trigliceridi can obrazuvaneto on Yes fatty brushes and sm″rt at hepatocitite. Nekrozata predizvikva v″zpalitelna format hroničen response under hepatit, kojto Mauger da premine in cirrhosis. Tak″v process nablûdava with hroničen alkoholiz″m CE. Hepatociti steatoza s″s da CE sreŝnat when you can virusen with hepatit and različni uvreždaniâ, toksični and lekarstveno included obusloven hepatit.

25. Dystrophia adiposa hepatis (Sudan III ).
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.