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Lecture notes, cheat sheets
Pathological anatomy. Lecture notes: briefly, the most important
Directory / Lecture notes, cheat sheets Table of contents
LECTURE No. 1. Pathological anatomy Pathological anatomy studies the structural changes that occur in the patient's body. It is divided into theoretical and practical. Structure of pathological anatomy: general part, particular pathological anatomy and clinical morphology. The general part studies general pathological processes, the patterns of their occurrence in organs and tissues in various diseases. Pathological processes include: necrosis, circulatory disorders, inflammation, compensatory inflammatory processes, tumors, dystrophies, cell pathology. Private pathological anatomy studies the material substrate of the disease, i.e., is the subject of nosology. Nosology (the study of the disease) provides knowledge of the etiology, pathogenesis, manifestations and nomenclature of diseases, their variability, as well as the construction of a diagnosis, the principles of treatment and prevention. Tasks of pathological anatomy: 1) study of the etiology of the disease (causes and conditions of the disease); 2) study of the pathogenesis of the disease (development mechanism); 3) the study of the morphology of the disease, i.e. structural changes in the body and tissues; 4) study of the morphogenesis of the disease, i.e. diagnostic structural changes; 5) study of the pathomorphosis of the disease (persistent cell change and morphological diseases under the influence of drugs - drug metamorphosis, as well as under the influence of environmental conditions - natural metamorphosis); 6) the study of complications of diseases, the pathological processes of which are not mandatory manifestations of the disease, but arise and worsen it and often lead to death; 7) study of disease outcomes; 8) study of thanatogenesis (mechanism of death); 9) assessment of the functioning and condition of damaged organs. Tasks of practical pathological anatomy: 1) control of the correctness and timeliness of the clinical diagnosis (autopsy). The percentage of discrepancy between the clinical and pathoanatomical diagnosis ranges from 12-19%. Causes: rare diseases with an erased clinical or laboratory picture; belated treatment of the patient in a medical institution. The timeliness of the diagnosis means that the diagnosis should be made within 3 days, in case of a serious condition of the patient - in the first hours; 2) advanced training of the attending physician (the attending physician is always present at the autopsy). For each case of discrepancy in diagnosis, the clinic conducts a clinical and anatomical conference, where a specific analysis of the disease takes place; 3) direct participation in the formulation of an intravital clinical diagnosis (by biopsy and examination of the surgical material). Methods for the study of pathological anatomy: 1) autopsy of the bodies of the dead; 2) biopsy (lifetime histological examination, carried out to diagnose and determine the prognosis of the disease). The research material is called "biopsy". Depending on how it is obtained, biopsies are classified as closed and hidden. Closed biopsies: 1) puncture (in the liver, kidneys, mammary glands, thyroid gland, lymph nodes, etc.); 2) aspiration (by suction from the bronchial tree); 3) trepanation (from dense bone tissue and cartilage); 4) diagnostic curettage of the uterine cavity, i.e. obtaining scrapings of the endometrium (used in obstetrics and gynecology); 5) gastrobiopsy (with the help of a gastrofibroscope, the gastric mucosa is taken). Hidden biopsies: 1) research of operational material (all material is taken); 2) experimental modeling of the disease. The structure of the biopsy can be liquid, solid or soft. In terms of timing, a biopsy is divided into planned (result on the 6-7th day) and urgent (result within 20 minutes, i.e. at the time of surgery). Methods for the study of pathoanatomical material: 1) light microscopy using special dyes; 2) electron microscopy; 3) luminescent microscopy; 4) radiography. Research levels: organismal, organ, systemic, tissue, cellular, subjective and molecular. Briefly about the history of pathological anatomy. In 1761, the Italian author G. Morgagni wrote the first work on pathological anatomy "On the location and causes of diseases identified by the anatomist." Of great importance for the development of pathological anatomy were the works of the French morphologists M. Bisha, J. Corvisart and J. Cruvelier, who created the world's first color atlas on pathological anatomy. R. Bayle was the first author of a complete textbook on private pathological anatomy, translated into Russian in 1826 by the doctor A.I. Kostomarov. K. Rokitansky was the first to systematize the pathological processes of body systems in various diseases, and also became the author of the first manual on pathological anatomy. In Russia, for the first time, autopsies began to be performed in 1706, when medical hospital schools were organized by order of Peter I. But the clergy prevented the autopsy. Only after the opening of the medical faculty at Moscow University in 1755, autopsies began to be carried out regularly. In 1849, the first department of pathological anatomy in Russia was opened. A. I. Polunin, I. F. Klein, M. N. Nikiforov, V. I. Kedrovskiy, A. I. Abrikosov, A. I. Strukov, V. V. Serov succeeded each other as the head of the department. LECTURE No. 2. The general doctrine of dystrophies Dystrophy is a pathological process that is a consequence of a violation of metabolic processes, with damage to cell structures and the appearance of substances in the cells and tissues of the body that are not normally determined. Dystrophies are classified: 1) by the scale of the prevalence of the process: local (localized) and general (generalized); 2) due to the occurrence: acquired and congenital. Congenital dystrophies have a genetic condition of the disease. Hereditary dystrophies develop as a result of a violation of the metabolism of proteins, carbohydrates, fats, in this case, the genetic deficiency of one or another enzyme that is involved in the metabolism of proteins, fats or carbohydrates matters. Later in the tissues there is an accumulation of incompletely converted products of carbohydrate, protein, fat metabolism. This process can develop in various tissues of the body, but the tissue of the central nervous system is necessarily damaged. Such diseases are called accumulation diseases. Children with these diseases die in the 1st year of life. The greater the lack of the necessary enzyme, the faster the development of the disease and the earlier death occurs. Dystrophies are divided into: 1) according to the type of metabolism that was disturbed: protein, carbohydrate, fat, mineral, water, etc .; 2) according to the point of application (according to the localization of the process): cellular (parenchymal), non-cellular (mesenchymal), which develop in the connective tissue, as well as mixed (observed both in the parenchyma and in the connective tissue). There are four pathogenetic mechanisms. 1. Transformation is the ability of some substances to transform into others having a similar structure and composition. For example, carbohydrates have this ability, transforming into fats. 2. Infiltration is the ability of cells or tissues to fill with an excessive amount of various substances. There are two types of infiltration. For infiltration of the first type, it is characteristic that a cell that participates in normal life receives an excess amount of a substance. After some time, there comes a limit when the cell cannot process, assimilate this excess. The infiltration of the second type is characterized by a decrease in the level of vital activity of the cell, as a result, it cannot even cope with the normal amount of the substance entering it. 3. Decomposition - characterized by the disintegration of intracellular and interstitial structures. There is a breakdown of protein-lipid complexes that are part of the membranes of organelles. In the membrane, proteins and lipids are in a bound state, and therefore they are not visible. But when the membranes break down, they are formed in the cells and become visible under a microscope. 4. Perverted synthesis - the formation of abnormal foreign substances in the cell, which are not formed during the normal functioning of the body. For example, in amyloid degeneration, cells synthesize an abnormal protein, from which amyloid is then formed. In patients with chronic alcoholism in the liver cells (hepatocytes), the synthesis of foreign proteins begins to occur, from which the so-called alcoholic hyaline is subsequently formed. Different types of dystrophies are characterized by their dysfunction of the tissue. With dystrophy, the disorder is twofold: quantitative, with a decrease in function, and qualitative, with a perversion of function, that is, features appear that are not characteristic of a normal cell. An example of such a perverse function is the appearance of protein in the urine in kidney diseases, when there are dystrophic changes in the kidney, or changes in liver tests that appear in liver diseases, and in heart diseases - a change in heart tones. Parenchymal dystrophies are divided into protein, fat and carbohydrate. Protein dystrophy is a dystrophy in which protein metabolism is disturbed. The process of dystrophy develops inside the cell. Among the protein parenchymal dystrophies, granular, hyaline-drop, hydropic dystrophies are distinguished. With granular dystrophy, during histological examination, protein grains can be seen in the cytoplasm of cells. Granular dystrophy affects parenchymal organs: kidneys, liver and heart. This dystrophy is called cloudy or dull swelling. This is related to macroscopic features. Organs with this dystrophy become slightly swollen, and the surface on the cut looks dull, cloudy, as if "scalded with boiling water." Contributes to the development of granular dystrophy for several reasons, which can be divided into 2 groups: infections and intoxications. A kidney affected by granular dystrophy increases in size, becomes flabby, a positive Schorr test can be determined (when the poles of the kidney are brought together, the kidney tissue is torn). On the section, the tissue is dull, the boundaries of the medulla and cortex are blurred or may be indistinguishable at all. With this type of dystrophy, the epithelium of the convoluted tubules of the kidney is affected. In normal tubules of the kidneys, even gaps are observed, and with granular dystrophy, the apical cytoplasm is destroyed, and the lumen becomes star-shaped. In the cytoplasm of the epithelium of the renal tubules are numerous grains (pink). Renal granular dystrophy ends in two variants. A favorable outcome is possible when the cause is eliminated, the epithelium of the tubules in this case returns to normal. An unfavorable outcome occurs with continued exposure to a pathological factor - the process becomes irreversible, dystrophy is transformed into necrosis (often observed in case of poisoning with kidney poisons). The liver with granular dystrophy is also slightly enlarged. When cut, the fabric acquires the color of clay. The histological sign of granular degeneration of the liver is the inconsistent presence of protein grains. It is necessary to pay attention to whether the beam structure is present or destroyed. With this dystrophy, proteins are divided into separately located groups or separately lying hepatocytes, which is called discomplexation of the hepatic beams. Cardiac granular dystrophy: the heart is also slightly enlarged outwardly, the myocardium becomes flabby, on the cut it resembles boiled meat. Macroscopically, protein grains are not observed. In histological examination, the criterion for this dystrophy is basophilia. Myocardial fibers differently perceive hematoxylin and eosin. Some areas of the fibers are intensely stained with hematoxylin in lilac, while others are intensely stained with eosin in blue. Hyaline droplet degeneration develops in the kidneys (the epithelium of the convoluted tubules is affected). It occurs in such kidney diseases as chronic glomerulonephritis, chronic pyelonephritis, and in case of poisoning. Drops of a hyaline-like substance are formed in the cytoplasm of cells. Such dystrophy is characterized by a significant violation of renal filtration. Hydropic dystrophy can occur in liver cells in viral hepatitis. At the same time, large light drops are formed in hepatocytes, often filling the cell. Fatty degeneration. There are 2 types of fats. The amount of mobile (labile) fats changes throughout a person's life, they are localized in fat depots. Stable (fixed) fats are included in the composition of cell structures, membranes. Fats perform a wide variety of functions - supporting, protective, etc. Fats are determined using special dyes: 1) sudan-III has the ability to stain fat orange-red; 2) scarlet colors red; 3) sudan-IV (osmic acid) stains fat black; 4) Nile blue has metachromasia: it stains neutral fats red, and all other fats turn blue or blue under its influence. Immediately before staining, the source material is processed using two methods: the first is alcohol wiring, the second is freezing. For the determination of fats, freezing of tissue sections is used, since fats dissolve in alcohols. Fat metabolism disorders are three pathologies: 1) proper fatty degeneration (cellular, parenchymal); 2) general obesity or obesity; 3) obesity of the interstitial substance of the walls of blood vessels (aorta and its branches). Actually fatty degeneration underlies atherosclerosis. The causes of fatty degeneration can be divided into two main groups: infections and intoxications. Nowadays, the main type of chronic intoxication is alcohol intoxication. Often there may be drug intoxication, endocrine intoxication - developing in diabetes. An example of an infection that provokes fatty degeneration is diphtheria, since diphtheria toxin can cause fatty degeneration of the myocardium. Fatty degeneration is observed in the same organs as protein - in the liver, kidneys and myocardium. With fatty degeneration, the liver increases in size, it becomes dense, on the cut it is dull, bright yellow. This type of liver received the figurative name "goose liver". Microscopic manifestations: fatty drops of small, medium and large sizes appear in the cytoplasm of hepatocytes. As a rule, they are located in the center of the hepatic lobule, but can occupy its entirety. There are several stages in the process of obesity: 1) simple obesity, when a drop occupies the entire hepatocyte, but when the impact of the pathological factor stops (when the patient stops drinking alcohol), after 2 weeks the liver returns to normal; 2) necrosis - an infiltration of leukocytes occurs around the focus of necrosis as a response to damage; the process at this stage is reversible; 3) fibrosis - scarring; the process goes into an irreversible cirrhotic stage. There is an increase in the heart, the muscle becomes flabby, dull, and if you carefully examine the endocardium, under the endocardium of the papillary muscles one can observe a transverse striation, which is called the "tiger heart". Microscopic characteristics: fat is present in the cytoplasm of cardiomyocytes. The process has a mosaic character - the pathological lesion extends to cardiomyocytes located along small veins. The outcome can be favorable when there is a return to normal (if the cause is eliminated), and if the cause continues to act, then cell death occurs, and a scar forms in its place. In the kidneys, fat is localized in the epithelium of the convoluted tubules. Such dystrophy occurs in chronic kidney diseases (nephritis, amyloidosis), in case of poisoning, general obesity. Obesity disrupts the metabolism of neutral labile fats, which are formed in excess in fat depots; body weight increases significantly as a result of the accumulation of fat in the subcutaneous fatty tissue, in the omentum, mesentery, in the perirenal, retroperitoneal tissue, in the tissue covering the heart. With obesity, the heart becomes, as it were, clogged with a thick fat mass, and then fat penetrates into the thickness of the myocardium, which causes its fatty degeneration. Muscle fibers undergo the pressure of the fatty stroma and atrophy, which leads to the development of heart failure. Most often, the thickness of the right ventricle is affected, as a result of which congestion develops in the systemic circulation. In addition, obesity of the heart can result in myocardial rupture. In literary sources, such a fat heart is characterized as Pickwick's syndrome. In the liver with obesity, fat can be formed inside the cells. The liver takes on the appearance of a "goose liver", as in dystrophy. It is possible to differentiate the resulting fat in the liver cells using color staining: Nile blue has the ability to stain neutral fat red in obesity, and blue in advanced dystrophy. Obesity of the interstitial substance of the walls of blood vessels (meaning the exchange of cholesterol): during infiltration from the blood plasma into the already prepared vascular wall, cholesterol enters, which is then deposited on the vascular wall. Some of it is washed back, and some is processed by macrophages. Macrophages loaded with fat are called xanthoma cells. Above the fat deposits, connective tissue grows, which protrudes into the lumen of the vessel, thus forming an atherosclerotic plaque. Causes of obesity: 1) genetically determined; 2) endocrine (diabetes, Itsenko-Cushing's disease); 3) hypodynamia; 4) overeating. Carbohydrate degeneration may be associated with impaired glycogen or glycoprotein metabolism. Violation of glycogen content is manifested in a decrease or increase in its amount in the tissues and the appearance where it is usually not detected. These disorders are expressed in diabetes mellitus, as well as in hereditary carbohydrate dystrophies - glycogenoses. In diabetes mellitus, there is insufficient consumption of glucose by tissues, an increase in its amount in the blood (hyperglycemia) and excretion in the urine (glucosuria). Tissue glycogen stores are drastically reduced. In the liver, there is a violation of the synthesis of glycogen, which leads to infiltration of its fats - fatty degeneration of the liver occurs. At the same time, inclusions of glycogen appear in the nuclei of hepatocytes, they become light ("perforated" and "empty" nuclei). With glucosuria, changes appear in the kidneys, manifested in the glycogen infiltration of the epithelium of the tubules. The epithelium becomes high, with light foamy cytoplasm; glycogen grains are also found in the lumen of the tubules. The tubules of the kidneys become more permeable to plasma proteins and sugars. One of the manifestations of diabetic microangiopathy develops - intercapillary (diabetic) glomerulosclerosis. Glycogenoses are caused by the absence or insufficiency of an enzyme that is involved in the breakdown of stored glycogen, and refers to hereditary fermentopathies (storage diseases). With carbohydrate dystrophies associated with a violation of the metabolism of glycoproteins, there is an accumulation of mucins and mucoids, also called mucous and mucus-like substances (mucosal degeneration). The causes are various, but most often it is inflammation of the mucous membranes. Systemic dystrophy underlies a hereditary systemic disease - cystic fibrosis. The endocrine apparatus of the pancreas, the glands of the bronchial tree, the digestive and urinary tracts, the biliary tract, the genital and mucous glands are affected. The outcome is different - in some cases, the regeneration of the epithelium and the complete restoration of the mucous membrane occur, while in others it atrophies, sclerosis, and the function of the organ is impaired. Stromal-vascular dystrophy is a metabolic disorder in the connective tissue, mainly in its intercellular substance, the accumulation of metabolic products. Depending on the type of impaired metabolism, mesenchymal dystrophies are divided into protein (dysproteinoses), fatty (lipidoses) and carbohydrate. Among dysproteinoses, mucoid swelling, fibrinous swelling, hyalinosis and amyloidosis are distinguished. The first three are associated with a violation of the permeability of the vascular wall. 1. Mucoid swelling is a reversible process. There are superficial shallow changes in the structure of the connective tissue. Due to the action of a pathological factor, decomposition processes occur in the main substance, i.e., the bonds of proteins and aminoglycans break up. Aminoglycans are free and found in connective tissue. Due to them, the connective tissue stains basophilically. There is a phenomenon of metachromasia (the ability of the fabric to change the color of the dye). So, toluidine blue is normally blue, and with mucoid swelling it is pink or lilac. Mucin (mucus) consists of proteins and therefore stains in a peculiar way. Glucosaminoglycans absorb well the fluid that comes out of the vascular bed, and the fibers swell, but do not collapse. The macroscopic picture is not changed. Factors that cause mucoid swelling include: hypoxia (hypertension, atherosclerosis), immune disorders (rheumatic disease, endocrine disorders, infectious diseases). 2. Fibrinoid swelling is a deep and irreversible disorganization of the connective tissue, which is based on the destruction of the basic substance of the tissue and fibers, accompanied by a sharp increase in vascular permeability and the formation of fibrinoid. May be due to mucoid swelling. The fibers are destroyed, the process is irreversible. The property of metachromasia disappears. The macroscopic picture is unchanged. Microscopically observed collagen fibers impregnated with plasma proteins, stained yellow with pyrofuchsin. The outcome of fibrinoid swelling can be necrosis, hyalinosis, sclerosis. Around the zone of fibrinoid swelling, macrophages accumulate, under the influence of which the cells are destroyed and necrosis occurs. Macrophages are able to produce monokines, which promote the reproduction of fibroblasts. Thus, the zone of necrosis is replaced by connective tissue - sclerosis occurs. 3. Hyaline degeneration (hyalinosis). Homogeneous transparent dense masses of hyaline (fibrillar protein) are formed in the connective tissue, which are resistant to alkalis, acids, enzymes, PAS-positive, well perceive acid dyes (eosin, acid fuchsin), pyrofuchsin stains yellow or red. Hyalinosis is the outcome of various processes: inflammation, sclerosis, fibrinoid swelling, necrosis, plasma impregnation. Distinguish between hyalinosis of vessels and connective tissue itself. Each can be widespread (systemic) and local. With vascular hyalinosis, mainly small arteries and arterioles are affected. Microscopically - hyaline is found in the subendothelial space, destroying the elastic plate, the vessel turns into a thickened vitreous tube with a very narrowed or completely closed lumen. Hyalinosis of small vessels is systemic, but significantly expressed in the kidneys, brain, retina, pancreas. Characteristic for hypertension, diabetic microangiopathy and diseases with impaired immunity. There are three types of vascular hyaline: 1) simple, resulting from insudation of unchanged or slightly changed blood plasma components (with hypertension, atherosclerosis); 2) lipogyalin containing lipids and β-lipoproteins (in diabetes mellitus); 3) complex hyaline, built from immune complexes, collapsing structures of the vascular wall, fibrin (typical for diseases with immunopathological disorders - for example, for rheumatic diseases). Hyalinosis of the connective tissue itself develops as a result of fibrinoid swelling, which leads to the destruction of collagen and impregnation of the tissue with plasma proteins and polysaccharides. The appearance of the organ changes, its atrophy occurs, deformation and wrinkling occur. The connective tissue becomes dense, whitish and translucent. Microscopically - the connective tissue loses fibrillarity and merges into a homogeneous dense cartilage-like mass; cellular elements are compressed and undergo atrophy. With local hyalinosis, the outcome is scars, fibrous adhesions of serous cavities, vascular sclerosis, etc. The outcome is unfavorable in most cases, but resorption of hyaline masses is also possible. 4. Amyloidosis - a kind of protein degeneration, which is a complication of various diseases (infectious, inflammatory or tumor nature). In this case, there is an acquired (secondary) amyloidosis. When amyloidosis results from an unknown etiology, it is primary amyloidosis. The disease was described by K. Rakitansky and was called "sebaceous disease", since the microscopic sign of amyloidosis is the sebaceous sheen of the organ. Amyloid is a complex substance - a glycoprotein, in which globular and fibrillar proteins are closely related to mucopolysaccharides. If proteins have approximately the same composition, then polysaccharides always have a different composition. As a result, amyloid never has a constant chemical composition. The proportion of proteins is 96-98% of the total mass of amyloid. There are two fractions of carbohydrates - acidic and neutral polysaccharides. The physical properties of amyloid are represented by anisotropy (the ability to birefringence, which is manifested in polarized light), under a microscope, amyloid produces a yellow glow, which differs from collagen and elastin. Colorful reactions for the determination of amyloid: the elective stain "Congo red" stains the amyloid in a brick red color, which occurs due to the presence of fibrils in the composition of the amyloid, which have the ability to bind and firmly hold the dye. Metachromatic reactions: iodine green, methyl violet, gentian violet stain amyloid red on a green or blue background. Staining occurs due to glycosaminoglycans. The most sensitive technique is fluorochrome treatment (thioflavin S, F). With this method, minimal amyloid deposits can be detected. There may be achromatic amyloid that does not stain completely; in this case, electron microscopy is used. Under an electron microscope, 2 components become visible: the F-component - fibrils and the P-component - periodic rods. Fibrils are two parallel threads, periodic rods consist of pentagonal formations. Allocate IV link of morphogenesis. I. Cellular transformation of the reticuloendothelial system, preceding the formation of cell clones - amyloidoblasts. II Synthesis by amyloidoblasts of the main component of amyloid - fibrillar protein. III Aggregation of fibrils with each other with the formation of an amyloid framework. IV. The connection of aggregated fibrils with blood plasma proteins, as well as with tissue glycosaminoglycans, which leads to the precipitation of an abnormal substance, amyloid, in the tissues. At the first stage, the formation of plasma cells in the organs of the reticuloendothelial system (plasmatization of the bone marrow, spleen, lymph nodes, liver). Plasmatization is also noted in the stroma of organs. Plasma cells are transformed into amyloid cells. Synthesis of fibrillar protein always occurs in cells of mesenchymal origin. These are lymphocytes, plasma cells, fibroblasts, reticular cells (fibroblasts are most often found in familial amyloidosis), plasma cells in primary amyloidosis (caused by a tumor), reticular cells in secondary amyloidosis. Also, Kupffer cells of the liver, stellate endotheliocytes, mesangial cells (in the kidney) can act as amyloidoblasts. When the protein accumulates enough, a scaffold is formed. Fibrillar protein is considered as foreign, abnormal. In response to its formation, an additional group of cells appears, which begins to try to lyse the amyloid. These cells are called amyloidoclasts. The function of such cells can be performed by free and fixed macrophages. For a long time, an equal struggle takes place between the cells that form and dissolve amyloid, but it always ends with the victory of amyloidoblasts, since immunological tolerance to the protein of amyloid fibrils occurs in the tissues. Proteins and polysaccharides are deposited on the fibrillar skeleton. Amyloid is always formed outside the cells and always has a close connection with connective tissue fibers: with reticular and collagen fibers. If the loss of amyloid occurs along the reticular fibers in the membranes of blood vessels or glands, then it is called perireticular amyloid (parenchymal) and is observed in the spleen, liver, kidneys, adrenal glands and intestines. If the formation and loss of amyloid falls on collagen fibers, then it is called pericollagen or mesenchymal. In this case, the adventitia of large vessels, the myocardial stroma, striated and smooth muscles, nerves and skin are affected. There are 3 old and 1 new modern theory that combines all three theories of the pathogenesis of amyloidosis. 1. Theory of dysproteinosis. According to this theory, dysproteinemia develops, with it there is an accumulation in the blood plasma of coarse protein fractions and abnormal proteins - paraproteins. They appear due to impaired protein metabolism. Then they go beyond the vascular bed, interact with tissue mucopolysaccharides. This theory is straightforward and does not explain the occurrence of dysproteinemia. 2. Immunological theory. In various diseases, decay products of tissues, leukocytes accumulate, bacterial toxins also circulate in the blood - all these substances have antigenic properties and lead to the formation of antibodies to themselves. An immune reaction develops to combine antigens with antibodies in those places where antibodies were produced, i.e., in the organs of the reticuloendothelial system. This theory explained only a part of amyloid degeneration, i.e., where there is chronic suppuration, and does not explain the genetic forms of amyloidosis. 3. Theory of cell-local synthesis. This theory studies amyloid as a secret of mesenchymal cells. 4. Universal theory - mutational. Mutagenic factors affect cells, thereby causing mutations, and a mechanism is triggered leading to the formation of amyloidoblast cells. There are secondary, or acquired, forms and idiopathic (primary), hereditary (familial, senile, tumor-like). The secondary form is a complication of a wide variety of infections. The causes of primary amyloidosis are unknown. Secondary amyloidoses are localized perireticularly, have a devastating effect on parenchymal organs. Secondary amyloids fall out along the course of collagen fibers. Most often, lesions of mesenchymal origin occur. In the idiopathic form, the heart, nerves, and intestines are affected. With hereditary or familial amyloidosis, there is an effect on the sympathetic nerve ganglia, as well as parenchymal organs - the kidneys. The so-called periodic illness is characteristic, which is observed in persons of the most ancient nationalities, for example, Jews, Arabs, Armenians. In the senile form, the heart and seminal vesicles are affected. Tumor-like amyloidosis is so named because the deposition of amyloid that occurs with it resembles a tumor. It affects the respiratory tract, trachea, bladder, skin, conjunctiva. Causes of secondary amyloidosis include: 1) chronic nonspecific lung diseases, such as chronic bronchitis with bronchiectasis, chronic lung abscesses, bronchiectasis; 2) tuberculosis in the cavernous form; 3) rheumatoid arthritis (about 25%). Macroscopic characteristics: organs are enlarged, dense, fragile, break easily, the edge of the incision is sharp, since amyloid is deposited under the vascular membrane, causing their narrowing, ischemia develops, and the organ becomes pale. Amyloid gives the body a characteristic greasy sheen. At autopsy on the organs, a macroscopic Virchow test for amyloid is used. The test is carried out on fresh, non-fixed organs: a plate is taken from the organ, washed with water from blood and watered with Lugol's solution, and after 30 minutes the organ is watered with 10% sulfuric acid. When dirty bottle staining appears, the test is positive. The spleen is affected in stage II. At the first stage, amyloid accumulates in the follicles of the spleen, in the white pulp, and looks like white grains. They look like sago grains, and such a spleen is called sago. In the second stage, amyloid spreads throughout the organ. The spleen greatly increases in size, dense consistency, brownish-red with a greasy sheen on the cut. She received the name greasy (ham) spleen. In the kidney, amyloid appears under the membrane of the glomerular capillaries, under the membrane of the vessels of the medulla and cortical layer, under the membranes of the convoluted and straight tubules, and also in the stroma of the kidney along the reticular fibers. This process is constant: the first stage - latent (latent) amyloid begins to form in the pyramids, in the glomerular blood vessels; the second stage is characterized by proteinuria. A large amount of protein is determined in the urine. In the stroma, the phenomena of sclerosis are noted - due to developing ischemia. In the epithelium, signs of fatty and hyaline-drop dystrophy are found. The third stage is nephrotic. Macroscopic changes correspond to a large sebaceous kidney: the organ is significantly enlarged in size, a thick and rather pale cortical layer with a greasy sheen and swollen purple-bluish pyramids. The microscopic picture shows that all glomeruli contain diffusely located amyloid. The last, final stage is uremic. At this stage, wrinkling of the kidney develops. Kidney failure leads to death. In the liver, amyloid deposition begins in the sinusoids between the Kupffer cells, along the reticular stroma of the lobules, the liver cells are compressed and die from atrophy. In the adrenal glands, amyloid is deposited only in the cortical layer along the capillaries, which leads to adrenal insufficiency, so any injury or stress can lead to death of the patient. In the intestine, the small intestine is most often affected. Amyloid is deposited along the reticular stroma of the mucosa, under the membrane of small vessels, which subsequently leads to atrophy and ulceration of the mucosa. There is a violation of absorption, depletion develops due to diarrhea. With lipidosis, there is a violation of the exchange of neutral fats, cholesterol or its esters. Obesity or obesity is an increase in the amount of neutral fats in fat depots. It is expressed in the abundant deposition of fat in the subcutaneous tissue, omentum, mesentery, mediastinum, epicardium. Adipose tissue appears where it is usually absent. Of great clinical importance is the developed obesity of the heart. Adipose tissue grows under the epicardium, envelops the heart, grows into the myocardial stroma and leads to atrophy of muscle cells. A heart rupture may occur. Obesity is divided into: 1) by etiology - into primary (idiopathic) and secondary (alimentary, cerebral, endocrine and hereditary); 2) according to external manifestations - on symmetrical, upper, middle and lower types of obesity; 3) by excess body weight - I degree (BMI 20-29%), II degree (30-49%), III degree (50-99%), IV degree (up to 100% or more). Violation of the metabolism of cholesterol and its esters underlies atherosclerosis. At the same time, in the intima of the arteries, not only cholesterol and its esters accumulate, but also low-density β-lipoproteins and blood plasma proteins, which is facilitated by an increase in vascular permeability. The accumulating macromolecular substances lead to the destruction of the intima, disintegrate and saponify. As a result, fat-protein detritus is formed in the intima, connective tissue grows, and a fibrous plaque is formed that narrows the lumen of the vessel. In carbohydrate stromal-vascular dystrophies, the balance of glycoproteins and glycosaminoglycans is disturbed. Collagen fibers are replaced by a mucus-like mass. The causes are dysfunction of the endocrine glands and exhaustion. The process can be reversible, but its progression leads to colliquation and necrosis of the tissue with the formation of cavities filled with mucus. Mixed dystrophies. Mixed dystrophies are spoken of in cases where the morphological manifestations of impaired metabolism accumulate both in the parenchyma and in the stroma, the wall of blood vessels and tissues. They occur when there is a violation of the metabolism of complex proteins - chromoproteins, nucleoproteins and lipoproteins, as well as minerals. 1. Violation of the exchange of chromoproteins (endogenous pigments). Endogenous pigments in the body perform a specific role: a) hemoglobin carries out oxygen transfer - respiratory function; b) melanin protects against UV rays; c) bilirubin is involved in digestion; d) lipofuscin provides the cell with energy in hypoxic conditions. All pigments, depending on the source of formation, are divided into hemoglobinogenic, proteinogenic and lipidogenic. Hemoglobin pigments consist of ferritin, hemosiderin and bilirubin. Hemosiderin is a pigment that is formed in a small amount under normal conditions during the natural aging of red blood cells and their decay. The decay products of erythrocytes are captured by cells of the reticuloendothelial system of the liver, spleen, bone marrow and lymph nodes, where they are presented in the form of brown grains of hemosiderin. Formed in sideroblasts that contain siderosomes. The basis of education is ferritin (iron protein), which is formed when combined with mucoproteins of the cell. Sideroblasts can retain it, but at high concentrations, the cells are destroyed and the pigment enters the stroma. Ferritin is detected by the Perls reaction (yellow blood salt in combination with hydrochloric acid becomes blue or blue-greenish). It is the only iron-containing pigment. The synthesis of this pigment is carried out in a living, functioning cell. A violation of this pigment is said when its amount increases sharply. There are general and local hemosiderosis. General hemosiderosis occurs with intravascular hemolysis of red blood cells. Causes - various infections (sepsis, malaria, etc.), intoxication (heavy metal salts, fluorine, arsenic) and blood diseases (anemia, leukemia, blood transfusion incompatible with the group or Rh factor). At the same time, the organs are enlarged in volume, compacted, brown or rusty in section. On microscopy of the liver, hemosiderin is found in the cells of the reticuloendothelial system in beams along the sinuses, as well as in hepatocytes, i.e., in the parenchyma. If the process is insignificant, then a complete structural and functional recovery is possible, and with a significant severity of the process, sclerosis and, as the final stage, cirrhosis. Local hemosiderosis develops with the breakdown of red blood cells outside the vascular bed, i.e., in the foci of hemorrhages. The most important are 2 localizations of hemosiderosis - in the substance of the brain and lungs. There are 2 types of hemorrhages: 1) small, diapedetic character; brain tissue is preserved, not destroyed, so hemosiderin will be formed both in the center and on the periphery of the hemorrhage focus; in the substance of the brain microglia and a small number of leukocytes; 2) hematoma type - when the walls of blood vessels are ruptured and are accompanied by the destruction of the substance of the brain; further a cavity (cyst) with brown (rusty) walls is formed; with such hemorrhages, hemosiderin is formed only on the periphery in the cyst wall. Hemosiderin appears in the focus of hemorrhage only at the end of the 2nd - beginning of the 3rd day. A hemorrhage in which it is not present is called fresh, and where it is present, it is called old. Hemosiderosis of the lungs or brown induration of the lungs, as hemosiderosis and sclerosis are combined in the lung. With chronic venous plethora in the pulmonary circulation, hypoxia occurs, leading to diapedesis of hemorrhages in the lung tissue. The pigment is located in the alveoli and the interalveolar septum, and hypoxia causes increased collagen production. The interalveolar septum thickens and thickens. Gas exchange and ventilation of the lungs are disturbed. Hematoidin is formed on the 10-12th day in very large and old foci of hemorrhage, which are accompanied by tissue destruction. It is always located in the center of the hearth. Morphological picture: crystals or rhomboid structures of yellow or pink color. Bilirubin is contained in the form of indirect, i.e. associated with albumin, or unconjugated. Bilirubin is taken up by liver hepatocytes, where it is conjugated with glucuronic acid, and such direct bilirubin enters the intestine. A violation is said to occur with an increase in its amount in the blood serum, followed by staining of the skin and mucous membranes in yellow. According to the mechanism of development, they differ: 1) hemolytic, or suprahepatic, jaundice, the causes of which are infections, blood diseases, intoxication, transfusion of incompatible blood; 2) parenchymal, or hepatic, jaundice - occurs due to liver disease; hepatocytes cannot fully capture indirect bilirubin and conjugate; 3) mechanical, or subhepatic, jaundice; causes - blockage of the common or hepatic ducts, papilla of Vater; tumor of the head of the pancreas, etc. Due to a violation of the outflow of bile, cholistasia occurs, which is accompanied by the expansion of capillaries in the lobules, thickening of the bile and the formation of bile clots. Hepatocytes begin to be infiltrated with bile pigments and destroyed, and the contents begin to enter the blood vessels. Thus, direct bilirubin enters the blood and intoxication and icteric staining occur. In addition, bile acids enter the bloodstream, causing itching and small pinpoint hemorrhages, which are associated with high vascular permeability. Outcomes: cholangitis (inflammation of the bile capillaries and ducts) and sclerosis, and then cirrhosis of the liver. Hemomelanin, or malarial pigment, occurs only in malaria, as it is produced by malarial plasmodium. It is introduced into erythrocytes, and then captured by cells of the reticuloendothelial system. The pigment has the appearance of black grains. The organs are enlarged, dense, grayish-black or slate in section. With an excess of pigment, aggregation of these grains occurs - malarial stasis. The consequence of stasis affects the central nervous system, there are areas of ischemia, followed by necrosis and small hemorrhages. In addition, there is a general hemosiderosis, as well as the development of hemolytic jaundice. Melanin is synthesized by melanocytes. Synthesis requires tyrosine and tyrosinase enzymes. Synthesis is regulated by the autonomic, endocrine systems and UV rays themselves. The vegetative (sympathetic) system increases production, while the parasympathetic decreases it. Endocrine system - adrenocorticotropic hormone stimulates, and melatonin depresses. The pigment is located in the basal layer of the epidermis. The ratio of melanocytes to all cells of the basal layer is 1: 15. The disorder follows the path of hyperproduction and hypoproduction. Hypermelanises, or bronze disease (Addison's disease), is an acquired disease in which there is increased diffuse staining of the skin, hypotension, adynamia, and muscle weakness. The disease is caused by damage to the adrenal glands (tuberculosis, amyloidosis, oncological processes). Under these conditions, ACTH is intensively synthesized. Pigmentary xeroderma is a congenital disease. The skin is dry, icteric, hyperemic, hyperpigmented and scaly. It occurs due to a lack of the enzyme endonuclease, which is involved in the utilization of melanin. Local hypermelanoses include birthmarks. This is a congenital malformation of the skin, which is characterized by the fact that in the process of embryogenesis there is a shift from the neuroectodermal tube of melanoblasts not only to the epidermis, but also to the dermis. Sometimes a birthmark can turn into a malignant tumor (melanoma). Among hypomelanosis, albinism, veitiligo and leukoderma are distinguished. Albinism is a congenital genetically determined pathology associated with the absence or insufficient production of the enzyme tyrotinase. Such people have white skin and hair, red eyes, impaired thermoregulation and barrier function of the skin. Life span is short. Veitiligo is an irregularly shaped area of depigmentation. This pathology is genetically determined and is hereditary. Leukoderma is a rounded area of depigmentation of the skin that has arisen as a result of exposure to pathogenic factors on the skin. Present in patients with syphilis, leprosy. With this pathology, skin lesions with destruction of Fatero-Pacino bodies (receptors) are noted. First, depigmentation appears on the skin of the neck and resembles a necklace of Venus. Depigmentation can be after burns, synthetic substances, etc. Lipofuscin is a pigment that looks like yellow granules and is localized in or near mitochondria. Normally, it is contained in hepatocytes, cardiocytes and ganglion cells, depositing oxygen; in conditions of hypoxia - provides the cell with oxygen. Under conditions of pathology, namely in chronic infections (for example, tuberculosis) and oncological processes, in the cells of the liver, heart and central nervous system, the amount of this pigment increases sharply and is localized in lysosomes. The function of depositing and providing cells with oxygen is not performed. The liver and heart decrease in size, become very dense, the color becomes brown-gray (brown). LECTURE No. 3. Necrosis Necrosis is a lifetime necrosis of cells and tissues of the body under the influence of various pathogenic factors. The basis of necrosis is apoptosis. Apoptosis is the natural and programmed death of a cell as a whole or part of it. It occurs under physiological conditions - this is natural aging (death of erythrocytes, Ti B-lymphocytes), with physiological atrophies (atrophy of the thymus, gonads, skin). Apoptosis can occur during pathological reactions (during the period of tumor regression), under the action of medicinal and pathogenic factors. Apoptosis mechanism: 1) condensation of the nucleus; 2) condensation and compaction of internal organelles; 3) cell fragmentation with the formation of apoptotic bodies. These are small organelles with eosinophilic cytoplasm with remnants of the nucleus. Then they are captured by phagocytes, macrophages, parenchyma and stroma cells. There is no inflammation. Morphogenesis of necrosis: 1) paranecrosis - dystrophy with a reversible character; 2) necrobiosis - dystrophic processes deepen and become irreversible; 3) cell death - the cell ends its functioning, the morphology is preserved; 4) autolysis or the stage of necrosis itself - all morphological signs are clearly visible. Autolysis is the process of cell destruction and self-digestion under the action of hydrolytic enzymes of its own structures, as well as under the action of proteolytic enzymes of leukocytes and macrophages. The exception is under the action of the thermal factor, when tissue charring occurs and this process is instantaneous, i.e., the manifestation of the 4th stage is immediately observed. The manifestation of necrosis depends on the strength and nature of the pathogenic factor, the state of the macroorganism itself. External (macroscopic) signs of necrosis: 1) the tissue structure in the necrosis zone is broken, the tissue is structureless; 2) the consistency of fabrics can be dense when the fabric is dry; this occurs when the tissue is rich in proteins and contains little water and the activity of hydrolytic enzymes is negligible (in the myocardium, liver, spleen and kidneys); the necrosis zone can be soft when the tissue contains a large amount of moisture, there is little protein, hydrolytic enzymes are active (brain, intestines); dry necrosis can turn into wet when infection occurs; 3) the color of the tissue in the area of necrosis may be black or dirty green (with gangrene), which is associated with the formation of pigment under the influence of putrefactive microbes; the appearance of a grayish mass has brain tissue, yellow-gray in tuberculosis and in the intestines, red or red-blue in pulmonary infarction; 4) the smell in the necrosis zone in gangrene is due to the fact that putrefactive microorganisms (Pseudomonas aeruginosa, clostridia) are able to produce hydrogen sulfide, which interacts with iron sulfide. Microscopic signs of necrosis: changes occur in the parenchyma and stroma. Karyopyknosis (densification of chromatin and reduction of the nucleus), karyorrhexis (disintegration of the nucleus into separate fragments) and karyolysis (the nucleus completely dissolves) occur in the nucleus. In the cytoplasm of cells, protein coagulation, plasmorhexis (breaking of the cytoplasm into separate fragments) and plasmolysis occur. In the stroma, under the action of active enzymes (collogenase and elastase), collagen structures are destroyed. They are impregnated with plasma proteins and fibrinoid necrosis occurs. Classification of necrosis Necrosis is classified as follows. 1. By etiology: 1) traumatic necrosis is caused by the action of various physical factors (high temperatures, concentrated alkalis and acids); 2) toxic necrosis is caused by bacterial toxins and chemical toxins (so acute renal failure can occur under the influence of salts, mercury, surrogates, medicinal substances); 3) trophoneurotic necrosis occurs with a decrease in vascular and nervous tissue trophism (bedsores); 4) vascular necrosis occurs when blood flow to tissues is stopped, with thromboembolism, thrombosis, with prolonged vasospasm and morphological phenomena of infarction (spleen, myocardium, brain, lungs, intestines, kidneys); 5) allergic necrosis is associated with the action of toxic immune complexes. 2. According to the mechanism of development: 1) direct necrosis - direct effect on the tissue of a pathogenic factor (traumatic, toxic); 2) indirect necrosis - due to the effect on the tissue of not the pathogenic factor itself, but indirectly through the vessels, nerves, etc. 3. According to clinical and morphological forms: 1) coagulative or dry necrosis: cheesy with tuberculosis and syphilis; waxy - in the muscles; fibrinoid in connective tissue disorders and in valves; 2) colliquational necrosis (in the substance of the brain and intestines) - a heart attack; 3) gangrene - tissue necrosis, which communicates with the external environment, is infected with putrefactive microbes with rejection of dead tissue as a result. Localization of gangrene: lower and upper limbs, internal organs that communicate with the external environment (lungs, large intestine, appendix, bladder and uterus). Gangrene can be dry or wet. For dry gangrene, circulatory disorders are necessary, for wet gangrene - venous stasis, edema, lymphostasis. LECTURE No. 4. Circulatory disorders Circulatory disorders are divided into 7 main options: 1) hyperemia, or plethora; 2) bleeding, or hemorrhage; 3) thrombosis; 4) embolism; 5) ischemia, or local anemia; 6) heart attack; 7) stasis. 1. Hyperemia Arterial hyperemia is not of great importance. Venous hyperemia is expressed in increased blood filling of the tissue, the difficulty in outflow of blood matters, while the arterial inflow does not change or is somewhat reduced. Venous hyperemia can be local and general, but general venous hyperemia is more common and of great practical importance. Microscopic characteristics: in the tissue of a living person there is a slight decrease in temperature (by 0,5-1 ° C), some expansion of the veins and capillaries, and a bluish color (cyanosis) appears on the skin. With rapidly developing venous congestion, tissue edema occurs, but it does not form in all tissues, but in cavities and those organs where there is space for fluid (in the kidneys and liver). At the same time, pulmonary edema, where there is a lot of space, is noticeable macroscopically. Transudate (edematous fluid) - occurs during venous stasis, often transparent, and the tissues that it washes are of an unchanged, normal color. Exudate is a fluid of plasma origin that occurs during inflammation. It is cloudy, grayish-yellow or red. Tissues bathed in exudate become dull. With slowly developing hyperemia, the tissue undergoes brown induration, since during chronic stagnation, when the volume of blood in the venous bed is increased, the permeability of the walls increases over time, which leads to the release of a small amount of fluid and the smallest formed elements into the surrounding tissue. In tissues, various pigments are released from erythrocytes: hemoglobin and hemosiderin. Induration is a compaction that occurs under conditions of chronic hypoxia. Any tissue of the body that falls into conditions of oxygen starvation begins to actively develop its stroma, and at the expense of connective tissue. An increase in the stroma is an adaptive reaction, since together with the stroma, capillaries grow in the tissue, which contributes to the compensation of hypoxia, in other words, sclerosis occurs. Microscopic picture: dilated and blood-filled venules. If there is acute venous stasis, then edematous fluid can be detected (does not contain protein, which differs from exudate, which contains more than 1% protein). It is cloudy due to the formed elements of the blood. In the lung tissue with alveolar septa, which normally has a "lace character", in pathology the gaps between the alveoli are filled with connective tissue, which somewhat presses the blood vessels. There is also a brown pigment - hemosiderin, part of which is found in macrophages. Local venous stasis: usually associated with blockage or occlusion of a major vein. There are 3 main types of general venous hyperemia: stagnation of the pulmonary circulation, stagnation of the systemic circulation, stagnation of the portal vein. Causes of stagnation in a small circle: left ventricular failure, mitral and aortic defects, compression of the mediastinum of the pulmonary veins by a tumor is the rarest cause. With acute venous stasis of the small circle, which develops from several minutes to several hours, pulmonary edema develops. Macroscopically: the lungs do not fall down, after pressing on them with a finger, unexpanded pits remain, when cut, a large amount of transudate and dark venous blood flow out. Microscopic picture: thickened alveolar septa, brown pigment is located partly freely in the septa, partly in macrophages, the veins are dilated with blood. Cause of death: cardiac and cardiopulmonary failure. Causes of stagnation of the systemic circulation: venous congestion in the pulmonary circulation, diffuse sclerotic changes in the lungs, right ventricular failure, compression of the trunks of the vena cava by the tumor. With rapidly developing stagnation, edema develops (with hyperemia of the systemic circulation - swelling of the skin and soft tissues), which is called anasarca. At the same time, the limbs increase, the outlines of the soft tissues change, when pressed on them, pits remain that do not straighten out, a venous pattern is visible. Forms of edema: edema of the abdominal cavity - ascites, edema of the pleural cavity - hydrothorax, edema of the pericardial cavity - hydropericardium, etc. Cyanosis is associated with varicose veins and is more pronounced, the farther the tissue is from the heart. "Nutmeg liver" is characterized by an increase in the liver: the lower edge extends from under the costal arch to several fingers, pain is noted on palpation. The size of the liver is much larger than normal. The section shows a distinct pattern of nutmeg. Microscopically, it is expressed in the fact that in the hepatic lobules all the main veins are dilated and filled with blood, all the capillaries that flow into them are also overflowing with blood, and fat appears in the peripheral parts of the lobules due to metabolic disorders. The cause of death is heart failure. Stagnation in the portal vein system is usually causally associated with the liver: diffuse sclerotic changes occur - cirrhosis, rarely congestive induration leads to the fact that capillaries in the hepatic lobules are compressed by connective tissue. Portal hypertension includes a number of clinical manifestations: 1) ascites; 2) varicose expansion of hepatic portocaval anastomoses (veins of the esophagus and stomach, veins of the rectum, veins of the anterior abdominal wall); 3) congestive enlargement of the spleen (splenomegaly) with further induration. 2. Bleeding Bleeding is the release of blood from the cavity of the heart and blood vessels into the environment or into the body cavity. Hemorrhage is a type of bleeding, which is characterized by the accumulation of blood in the tissues. Possible internal bleeding into the cavity (hemopericarditis, hemarthrosis, hemothorax, etc.). By prescription, hemorrhages are divided into old (in the presence of hemosiderin) and fresh. According to the type of tissue changes, they differ: 1) hematoma-type hemorrhages - always accompanied by tissue destruction; 2) petechiae, or ecchymosis - small pinpoint hemorrhages that are localized on the skin or mucous membranes; 3) hemorrhagic infiltration, or impregnation; does not cause tissue destruction; 4) bruising. Mechanisms of hemorrhage: rupture of the wall, separation of the wall and diapedesis of erythrocytes. Outcome: a hematoma in the substance of the brain is converted into a cyst, which contains serous contents. In soft tissues, the hematoma resolves or suppurates. 3. Thrombosis Thrombosis is a process of intravital blood coagulation in the lumen of a vessel or in the cavities of the heart. This is the irreversible denaturation of proteins and blood cells. The reasons: 1) changes in the vascular wall during inflammatory processes, angioedema, atherosclerosis, and hypertension (instead of proper constriction and dilatation, the venous vessel narrows and maintains its spastic shape for a long time); 2) changes in the speed and direction of blood flow (with heart failure). Thrombi that appear with a sharp contractile weakness, with increasing heart failure, are called marantic (congestive). They can occur in peripheral veins; 3) a number of reasons associated with a change in the chemical composition of the blood: with an increase in coarse proteins, fibrinogen, lipids. Such conditions are observed in malignant tumors, atherosclerosis. The mechanism of thrombus formation consists of IV stages: I - phase of platelet agglutination; II - fibrinogen coagulation, fibrin formation; III - agglutination of erythrocytes; IV - precipitation - sedimentation in clots of various plasma proteins. Macroscopically - it is necessary to distinguish a thrombus from a post-mortem clot. The thrombus has a close connection with the wall of the blood vessel, and the clot, as a rule, lies freely. A thrombus is characterized by a dull, sometimes even rough surface, while a clot has a smooth, shiny, “mirror-like” surface. The thrombus has a fragile texture, and the consistency of the clot is jelly-like. Depending on the place and conditions under which the formation of a thrombus occurred, there are: 1) white blood clots (platelets, fibrins, leukocytes). These clots form when there is fast blood flow in the arteries; 2) red blood clots (platelets, fibrins, erythrocytes) occur in conditions of slow blood flow, most often in the veins; 3) mixed: the place of attachment is called the head, the body is freely located in the lumen of the vessel. The head is often built on the principle of a white blood clot, the body has an alternation of white and red areas, and the tail is usually red; 4) hyaline thrombi - a very rare variant (they consist of destroyed erythrocytes, platelets, protein precipitate). It is the protein precipitate that creates a resemblance to cartilage. These thrombi form in arterioles and venules. In relation to the lumen of the vessel, thrombi are distinguished: 1) clogging (obturating), i.e., the lumen of the vessel is closed by a mass of a blood clot; 2) parietal; 3) in the chambers of the heart and in aneurysms there are spherical thrombi. Outcomes: 1) the most frequent - organization, i.e., germination of connective tissue occurs; 2) petrification - deposition of lime; 3) secondary softening (colliquation) of a thrombus - develops due to two reasons: microbial fermentolysis (when microbes enter the thrombus) and local fermentolysis, which develops due to its own enzymes released when damaged. 4. Embolism An embolism is the transfer of particles by the blood that are not normally observed in it. There are three central directions of movement of emboli in the circles of blood circulation: 1) from the left heart to the arterial system; 2) from the veins of the systemic circulation through the right heart into the pulmonary trunk; 3) along the portal vein. There are 7 types of embolisms. 1. Thromboembolism: the cause of a thrombus detachment is its softening, but it can also come off on its own from the attachment site. 2. Tissue (cellular) embolism is observed in malignant tumors, when cancer or sarcoma cells grow into the bloodstream, the cells detach from the tumor and circulate with the blood stream; when stuck in the distant branches of the internal organs, they cause tumor embolism. These distant tumor nodules in relation to the maternal tumor are metastases, and the process itself is called metastasis. In gastric cancer, metastasis occurs through the portal vein to the liver. 3. Microbial embolism develops with purulent inflammation. With the help of its enzymes, pus melts the surrounding tissues, including blood vessels, microbes get the opportunity to penetrate into the blood through the melted vessel and circulate throughout the body. The larger the abscess, the more likely the introduction of microbes into the blood. The condition that is observed in this case is called sepsis. 4. Fat embolism develops with large-scale fractures of tubular bones with crushing. Fat droplets (from the bone marrow) enter the veins and obliterate the capillaries of the lungs. 5. Air embolism occurs when large veins are injured. 6. Gas embolism occurs during decompression sickness (for example, divers rise sharply) - the gas composition of the blood changes, nitrogen bubbles begin to appear spontaneously in it (at high pressure - as a rule, during diving - nitrogen is converted in the blood to a greater extent, and when rising, nitrogen does not have time to leave the blood). 7. Embolism by foreign bodies - when bullets and fragments move against the flow of blood under the influence of gravity (retrograde) or along the bloodstream. 5. Heart attack An infarction is a necrosis resulting from the cessation of the blood supply to the tissue; infarctions are distinguished by color white, red and white with a red rim. According to the shape, which is associated with the type of blood circulation, there are irregular and conical (in the kidneys, lungs). The consistency can be dry and wet. Stages of development of a heart attack. 1. The ischemic stage does not have a macroscopic picture and most often lasts several hours (up to 8-10 hours). Microscopically: disappearance of glycogen and important enzymes in cells. 2. The stage of necrosis - macro- and microscopically, the infarction has a characteristic expression. The duration of the stage is up to a day. 3. Exit stage - often ends with organization. In the brain, a cavity is formed - a cyst, in the heart and other organs there is an organization and formation of a scar. This takes a week or more. 6. Staz Stasis is a stoppage of blood flow in the vessels of the microcirculatory circle, resulting in hemolysis and blood clotting. The reason is dyscirculatory disorders, which may be associated with the action of physical and chemical factors - with infectious, infectious-allergic and autoimmune diseases, with diseases of the heart and blood vessels. Stasis is reversible and irreversible (leading to necrosis) in nature. LECTURE No. 5. Inflammation Inflammation is a complex protective stromal-vascular reaction of the body in response to the action of a pathological factor. According to the etiology, 2 groups of inflammations are distinguished: 1) banal; 2) specific. Specific is inflammation, which is caused by certain causes (pathogens). This is inflammation caused by Mycobacterium tuberculosis, inflammation in leprosy (leprosy), syphilis, actinomycosis. Inflammations caused by other biological factors (E. coli, cocci), physical, chemical factors are banal inflammations. According to the time of the course of inflammation, there are: 1) acute - lasts 7-10 days; 2) chronic - develops from 6 months or more; 3) subacute inflammation - the duration is between acute and chronic. According to morphology (pathoanatomical classification), exudative and proliferative (productive) inflammation are distinguished. The causes of inflammation can be chemical, physical or biological. The phases of inflammation are alteration, proliferation and exudation. In the phase of alteration, tissue damage occurs, which pathologically manifests itself in the form of destruction and necrosis. Activation and release of biologically active substances take place, i.e. mediation processes are launched. Mediators of inflammation of cellular origin are mast cells, platelets, basophils, lymphocytes and monocytes; mediators of plasma genesis - collecrein-kinin system, complementary, clotting and anti-clotting systems. The actions of these mediators affect the course of the next phase of inflammation - exudation. Mediators increase the permeability of the vessels of the microvasculature, activate leukocyte chemotaxis, intravascular coagulation, secondary alteration in the very focus of inflammation and the activation of immune mechanisms. During exudation, arterial and venous hyperemia occurs in the focus of inflammation, and the permeability of the vascular wall increases. Therefore, fluid, plasma proteins, and also blood cells begin to pass into the focus of inflammation. Intravascular coagulation occurs with deformation of the vessels in the outlet vessels of the focus of inflammation, and thus the focus is isolated. Proliferation is characterized by the fact that in the focus of inflammation, blood cells accumulate in large quantities, as well as cells of histogenic origin. Neutrophils appear after a few minutes. Leukocytes perform the function of phagocytosis. Neutrophils after 12 hours lose glycogen, fill with fat and turn into purulent bodies. Monocytes that have left the vascular bed are macrophages (simple and complex) that are capable of phagocytosis. But they have little or no bactericidal protein cations, so macrophages do not always carry out complete phagocytosis (endocytobiosis), that is, the pathogen is not destroyed from the body, but is absorbed by the macrophage. There are three types of macrophages. Simple macrophages are transported to epithelioid cells, they are elongated, have a single nucleus and look like an epithelium (in tuberculosis). Giant cells, which are 15-30 times larger than usual, arise by the fusion of several epithelioid cells. They are round in shape, and the nuclei are clearly located on the periphery and are called Pirogov-Langhans cells. The giant cell of foreign bodies can instantly transform into histiocytes. They are round and the nuclei are located in the center. Exudative inflammation is inflammation in which exudative processes predominate. Occurrence conditions: 1) the impact of damaging factors on the vessels of the microvasculature; 2) the presence of special factors of pathogenicity (pyogenic flora, isolation of chemotaxis); distinguish between independent and non-independent types of exudative inflammation. Independent species occur on their own, and non-independent species join them. Independent include serous inflammation, fibrinous and purulent. To dependent - catarrhal, hemorrhagic and putrefactive inflammation. Mixed inflammation is also distinguished - this is a combination of at least 2 types of inflammation. Serous inflammation is characterized by the accumulation of the liquid part of the exudate containing about 2,5% protein and various cellular forms (platelets, leukocytes, macrophages) and cells of local tissues. The exudate is similar to the transudate that occurs with venous congestion, heart failure. The difference between exudate and transudate is that the presence of protein provides a special optical effect of Gindal - opalescence, i.e., the glow of a colloidal solution in transmitted light. Localization everywhere - in the skin, mucous membranes, serous membranes and in the parenchyma of organs; for example, second-degree burns that form blisters. In the serous cavities, fluid accumulations are called exudative pericarditis, pleurisy, and peritonitis. The membranes themselves are edematous, plethoric, and between them there is a liquid. Parenchymal organs become enlarged, flabby, on the cut the tissue is dull, gray, resembling boiled meat. Microscopic views: expanded intercellular spaces, gaps between cells, cells are in a state of dystrophy. The exudate compresses the organs, disrupting their function. But basically the outcome is favorable, sometimes you have to release large amounts of exudate. The outcome of serous inflammation in parenchymal organs is diffuse small-focal sclerosis and functional disorders. Fibrinous inflammation: exudate is represented by fibrinogen. Fibrinogen is a blood protein that, going beyond the blood vessels, turns into insoluble fibrin. Intertwining fibrin threads form on the surfaces of the organs of the film - grayish, of various thicknesses. Occurs on the mucous membranes, serous membranes, as well as on the skin. Depending on how the film is connected to the surface, there are croupous (formed on mucous membranes lined with a single-layer epithelium) - if the film is easily separated from the underlying tissue and diphtheria (on stratified epithelium) - if the film is poorly separated. The outcome of fibrinous inflammation depends on the type of inflammation. Croupous films are characterized by easy detachment, while the basement membrane does not suffer, complete epithelialization occurs. On serous membranes - rejection of the film into the cavity, which does not always have time to be resorbed by macrophages, and organization occurs. As a result, fibrous adhesions are formed between the parietal and visceral sheets of the corresponding serous membrane - adhesions that limit the mobility of organs. If films have formed in the breathing tube, then when rejected, they are able to clog its lumen, thereby causing asphyxia. Such a complication is a true croup (occurs, in particular, with diphtheria). It is necessary to distinguish it from a false croup that develops with stenosis of the respiratory tube with edema, most often of an allergic nature, with SARS. Diphtheria also generally has an anatomically favorable outcome. With diphtheria, "tiger heart", severe parenchymal myocarditis can be observed. Sometimes under the films there is the formation of deep defects - erosion, ulcers. With purulent inflammation, the exudate is represented by polymorphonuclear leukocytes, includes dead leukocytes, destroyed tissues. Color from white to yellow-green. ubiquitous localization. The reasons are varied; First of all - coccal flora. The pyogenic flora includes staphylo- and streptococci, meningococci, gonococci and coli - intestinal, Pseudomonas aeruginosa. One of the factors of the pathogenicity of this flora are the so-called leukocidins, they cause an increase in the chemotaxis of leukocytes on themselves and their death. In the future, with the death of leukocytes, factors that stimulate the chemotaxis of new leukocytes in the focus of inflammation occur. Proteolytic enzymes, which are released during destruction, are able to destroy both their own tissues and tissues of the body. Therefore, there is a rule: "you see pus - let it out" in order to prevent the destruction of your own tissues. There are the following types of purulent inflammation. 1. Phlegmon - diffuse, diffuse, without clear boundaries, purulent inflammation. Diffuse infiltration by leukocytes of various tissues occurs (most often - subcutaneous fat, as well as the walls of hollow organs, intestines - phlegmonous appendicitis). Phlegmonous inflammation can occur in the parenchyma of any organs. 2. Abscess - focal, delimited purulent inflammation. Allocate acute and chronic abscess. An acute abscess has an irregular shape, an indistinct, blurred border, and there is no decay in the center. A chronic abscess has a regular shape, with clear boundaries and a decay zone in the center. The clarity of the border is due to the fact that the connective tissue grows along the periphery of the abscess. In the wall of such an abscess, several layers are distinguished - the inner layer is represented by a pyogenic membrane of granulation tissue, and the outer part of the wall is formed by fibrous connective tissue. When an abscess is connected to the external environment with the help of anatomical channels (in the lungs), an air space is formed in the cavity, and the pus is located horizontally (this is noticeable on the x-ray). 3. Empyema - purulent inflammation in the anatomical cavities (empyema of the pleura, maxillary sinuses, gallbladder). The outcome of purulent inflammation depends on the size, shape, localization of foci. Purulent exudate can resolve, sometimes sclerosis develops - scarring of the tissue. A complication in the form of erosion of surrounding tissues by proteolytic enzymes can lead to the formation of fistulas - channels through which the abscess is emptied outward (self-cleaning) or into the serous membrane (for example, a lung abscess can lead to the development of pleural empyema, liver - to purulent peritonitis, etc. ); bleeding; exhaustion; intoxication, etc. Catarrhal inflammation - mucus is mixed with the exudate. There is a drain of exudate from the inflamed surface. Typical localization - mucous membranes. The outcome of catarrhal inflammation is the complete restoration of the mucosa. In chronic catarrhs, atrophy of the mucous membrane is possible (atrophic chronic rhinitis). Hemorrhagic inflammation is characterized by the admixture of red blood cells to the exudate. The exudate becomes red, then, as the pigments are destroyed, it becomes black. It is typical for viral infections, such as influenza, measles, natural (black) smallpox, with endogenous intoxications, for example, intoxication with nitrogenous slags in chronic renal failure. It is typical for pathogens of especially dangerous infections that are strong in virulence. Putrid (gangrenous) inflammation occurs as a result of the attachment of putrefactive flora, primarily fusospirochetal, to the foci of inflammation. It is more common in organs that have a connection with the external environment: putrefactive gangrene of the lung, limbs, intestines, etc. Decaying tissues are dull, with a fetid specific odor. Mixed inflammation. They talk about it when there is a combination of inflammation (serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic). Productive (proliferative inflammation) - the proliferation phase predominates, resulting in the formation of focal or diffuse cellular infiltrates, which can be polymorphic-cellular, lymphocytic-cell, macrophage, plasma-cell, giant-cell and epithelioid-cell. One of the main conditions for the development of proliferative inflammation is the relative stability of damaging factors in the internal environment of the body, the ability to persist in tissues. Features of proliferative inflammation: 1) chronic undulating course; 2) localization mainly in connective tissues, as well as in tissues whose cells have the ability to proliferate - the epithelium of the skin, intestines. In morphology, the most characteristic feature is the formation of granulation tissue. Granulation tissue is young, immature, growing connective tissue. Its formation is determined by classical biological properties. The growth and functioning of tissue are antagonistic processes. If the tissue begins to function well, then its growth slows down, and vice versa. Macroscopically, the granulation tissue is red, with a shiny granular surface and is prone to bleeding. The main substance is translucent, therefore, capillaries filled with blood shine through it, hence the red color. The fabric is granular, as the knees lift the main substance. Varieties of productive inflammation: 1) interstitial, or interstitial; 2) granulomatous; 3) productive inflammation around parasitic animals; 4) hypertrophic growths. Intermediate inflammation usually develops in the stroma of parenchymal organs; is diffuse. It can occur in the interstitium of the lungs, myocardium, liver, kidneys. The outcome of this inflammation is diffuse sclerosis. The function of organs in diffuse sclerosis deteriorates sharply. Granulomatous inflammation is a focal productive inflammation in which foci arise in the tissue from cells that have the ability to phagocytosis. These lesions are called granulomas. Granulomatous inflammation occurs in rheumatism, tuberculosis, occupational diseases - when various mineral and other substances are deposited on the lungs. Macroscopic picture: the granuloma is small, its diameter is 1-2 mm, it is barely visible to the naked eye. The microscopic structure of the granuloma depends on the phase of differentiation of phagocytic cells. The precursor of phagocytes is considered to be a monocyte, which differentiates into a macrophage, then into an epithelioid cell, and then into a giant multinucleated cell. There are two types of multinucleated cells: the foreign body giant cell and the Pirogov-Langhans giant multinuclear cell. Granulomas are divided into specific and nonspecific. A specific variant of productive granulomatous inflammation is called specific, which is caused by specific pathogens and which develops on an immune basis. Specific pathogens are mycobacterium tuberculosis, pale treponema, actinomycete fungi, mycobacterium leprosy, causative agents of rhinoscleroma. Features of specific inflammation: 1) chronic undulating course without a tendency to self-heal; 2) the ability of pathogens to cause the development of all 3 types of inflammation, depending on the state of the organism's reactivity; 3) a change in inflammatory tissue reactions due to a change in the immunological reactivity of the body; 4) in morphological terms, inflammation is characterized by the formation of specific granules, which have a characteristic structure depending on the pathogen. Inflammation in tuberculosis: Mycobacterium tuberculosis is capable of causing alterative, exudative, proliferative inflammation. Alternative inflammation develops most often with hypoergy, which is caused by a decrease in the body's defenses. Morphologically it is manifested by caseous necrosis. Exudative inflammation usually occurs in conditions of hyperergy - increased sensitivity to antigens, toxins of mycobacteria. Mycobacterium, when it enters the body, is able to persist there for a long time, in connection with this, sensitization develops. Morphological picture: foci are localized in various organs and tissues. Initially, serous, fibrinous or mixed exudate accumulates in the foci, later the foci undergo caseous necrosis. If the disease is detected before caseous necrosis, then treatment can lead to resorption of the exudate. Productive inflammation develops under conditions of specific tuberculous non-sterile immunity. The morphological manifestation will be the formation of specific tuberculous granules (in the form of "millet grain"). Microscopically: the miliary focus is formed by epithelioid cells and Pirogov-Langhans giant cells. On the periphery of the granuloma are usually numerous lymphocytes. Immunologically, these granulomas reflect delayed-type hypersensitivity. Outcome: usually caseous necrosis. Most often in the center of the granuloma is a small foci of necrosis. Macroscopic classification of foci of tuberculous inflammation Foci are classified into 2 groups: miliary and large. Miliary foci are most often productive, but may be alterative and exudative. From the large foci, there are: 1) acinous; macroscopically, it resembles a shamrock, as it consists of three stuck together miliary foci; there are also productive and alternative; 2) caseous focus - in size it is similar to a mulberry or raspberry. Black color. Inflammation is basically always productive, pigments adsorb connective tissue; 3) lobular; 4) segmental; 5) lobar foci. Lobar foci are exudative foci. Outcomes - scarring, rarely necrosis. In exudative foci - encapsulation, petrification, ossification. For large foci, the formation of a secondary colliquation is characteristic, and the liquefaction of dense masses occurs. Liquid masses are able to be emptied, cavities remain outside and in place of these foci - cavities. Inflammation in syphilis. There are primary, secondary, tertiary syphilis. Primary syphilis - inflammation is most often exudative, as it is caused by hyperergic reactions. Morphological picture: the manifestation of a hard chancre at the site of the introduction of the spirochete - an ulcer with a shiny bottom and dense edges. The density depends on the massiveness of the inflammatory cell infiltrate (from macrophages, lymphocytes, fibroblasts). The chancre usually scars. Secondary syphilis lasts from several months to several years and is accompanied by an unstable state of restructuring of the immune system. There is also a hyperergic reaction at the base, so the inflammation is exudative. Characterized by spirochetemia. Secondary syphilis occurs with relapses, in which rashes are observed - exanthema on the skin and enanthema on the mucous membranes, which disappear without a trace (without scarring). With each relapse, specific immune reactions develop, as a result, the number of rashes decreases. Inflammation becomes productive in the 3rd phase of the disease - with tertiary syphilis. Formed specific syphilitic granulomas - gummas. Macroscopically, in the center of the syphilitic gumma there is a focus of glutinous necrosis, around it there is a granulation tissue with a large number of vessels and cells - macrophages, lymphocytes, plasma cells, along the periphery there is granulation tissue, which passes into scar tissue. Localization everywhere - intestines, bones, etc. The outcome of the gum is scarring with disfigurement (gross deformation of the organ). The second variant of the course of productive inflammation in tertiary syphilis is interstitial (interstitial) inflammation. The most common localization in the liver and in the aorta is syphilitic aortitis. Macroscopic picture: aortic intima looks like shagreen (finely dressed) skin. Microscopically, diffuse gummous infiltration is noticeable in the media and adventitia, and with differential staining methods, destruction of the elastic framework of the aorta. The outcome is a local expansion (aortic aneurysm), which can rupture, and a blood clot can also form. Nonspecific granulomas have no characteristic features. They are found in a number of infectious (with rheumatism, typhus, typhoid fever) and non-infectious diseases (with sclerosis, foreign bodies). The outcome is twofold - scarring or necrosis. The scar is formed small, but since the disease is chronic, like rheumatism, the number of scars increases with each new attack, hence the degree of sclerosis increases. In rare cases, granulomas undergo necrosis, which indicates an unfavorable course of the disease. Productive inflammation around parasitic animals Parasites are Echinococcus, Cysticec, Trichinella, etc. Around the invading parasites that have a capsule, granulation tissue grows, rich in macrophages and giant cells of foreign bodies. The outcome is sclerosis, scarring with the formation of a fibrous capsule around the parasite. The organism cannot destroy the parasite and tries to isolate itself from it. Hypertrophic growths are polyps and condylomas. These formations are formed during chronic inflammation, in which connective tissue and epithelium are involved. Polyps most often develop in the mucous membrane of the colon, in the stomach, in the nasal cavity, and condylomas - on the skin, near the anus and genital tract. Both of them resemble a tumor, but they do not belong to them, although it is possible to transform polyps and warts into a tumor, first benign, and then malignant. Hypertrophic formations differ from tumors by the presence of inflammatory infiltration in their stroma. Hypertrophic formations are removed with the help of operations, it is important to treat the underlying disease. LECTURE No. 6. Immunopathological processes Immunopathology studies the processes and diseases resulting from immune conflict and the disturbance of immunological homeostasis. The immune response can be specific and non-specific. The nonspecific immune response consists of mechanical protection, humoral and cellular mechanisms. Mechanical protection is the first barrier to pathogenesis and is carried out by the epithelial cover due to the movement of cilia (cough, vomiting, sneezing, peristalsis, lacrimal fluid, etc.). The humoral mechanism is provided by the ability of body fluids to kill the pathogen. So, blood, saliva, lacrimal fluid, intestinal secretion are rich in lysocine, interferon, antibacterial substrates. Cellular immunity functions through cells such as neutrophils, basophils, macrophages, Kupffer cells, and others that are capable of phagocytosis. The specific immune response is composed of specificity, immune memory, and recognition. Specificity is protection only against a specific pathogen. Memory is the property of the body to maintain immunity throughout subsequent life as a defense against re-infection. Friend-or-foe recognition is the ability to differentiate one's tissues from those of others and produce antibodies to foreign cells. Immune reactions are divided into humoral and cellular (central and peripheral). The central ones include the thymus gland, bone marrow, tonsils and a group of lymph nodes of the internal organs. To peripheral - lymph nodes, spleen, blood and reticulo-endothelial system. The main functions of the thymus gland are lymphopoietic, immunoregulatory and endocrine, which are carried out due to the secretion of hormones by its epithelial cells - thymosin, thymopoietin, thymic serum factor, etc. Its indirect effect on immunogenesis is carried out due to the endocrine system and regulatory T-lymphocytes (effectors, helpers and suppressors). During life, the thymus gland undergoes age-related involution - it is replaced by fatty tissue, as a result of which cellular immunity decreases, infectious, autoimmune and oncological diseases become more frequent. Pathology of the thymus: 1) aplasia, hypo- and dysplasia are congenital anomalies; 2) accidental involution - a rapid decrease in its mass and volume under the influence of glucocorticosteroids in various stressful situations, with infections, intoxications and injuries; 3) atrophy is the cause of a part of acquired immunodeficiency syndromes (with chronic infectious diseases, with immunosuppressive therapy); microscopically - the parenchyma of the gland decreases in volume, thymic bodies calcify, connective and adipose tissue grows in the perivascular spaces; 4) thymomegaly is characterized by an increase in the mass and volume of the parenchyma while maintaining its normal structure; it can be congenital and acquired (with chronic adrenal insufficiency); hormone production is reduced; 5) thymus hyperplasia with lymphoid follicles is characteristic of autoimmune diseases; in sharply expanded intralobular perivascular spaces of the parenchyma, B-lymphocytes and plasma cells accumulate, lymphoid follicles appear; hormone production can be reduced or increased. The most characteristic changes in the peripheral lymphoid tissue and spleen during antigenic stimulation and its hereditary insufficiency. With antigenic stimulation of the body, changes are expressed by a macrophage reaction and hyperplasia of lymphocytes, followed by their plasmacytic transformation. In the lymph nodes, which increase, become full-blooded and edematous, in their cortical layer, in the light centers of the follicles and the medulla, a large number of plasmablasts and plasma cells appear. They crowd out lymphocytes. There is proliferation and desquamation of sinus cells, the formation of a large number of macrophages and protein-polysaccharide substances in the stroma. The spleen is enlarged, looks full-blooded and juicy, large follicles are clearly visible on its section. There is hyperplasia and plasmatization of both the red pulp and especially the follicles of the spleen, the peripheral zone of which consists entirely of plasmablasts and plasma cells. In the red pulp, along with plasmablasts, there are many macrophages. Hereditary insufficiency of peripheral lymphoid tissue is characterized by both changes in the spleen and (especially) lymph nodes. In the spleen, the size of the follicles is significantly reduced, there are no light centers and plasma cells. There are no follicles and cortical layer in the lymph nodes. Forms of specific reactions that make up immunology: antibody production, immediate-type hypersensitivity, delayed-type hypersensitivity, immunological memory and immunological tolerance. An immediate type hypersensitivity reaction has the morphology of acute immune inflammation. It is characterized by the speed of development, the predominance of alternative and vascular-exudative changes, the slow course of reparative processes. Alternative changes are characteristic of vessels, ground substance and fibrous structures of the connective tissue. They are represented by plasma impregnation, mucoid and fibrinoid swelling, fibrinoid necrosis. Coarsely dispersed proteins, fibrin, neutrophils, immune complexes and erythrocytes appear in the focus of inflammation. In this regard, the most characteristic (for an immediate hypersensitivity reaction) are fibrinous and fibrinous-hemorrhagic exudates. Proliferative-reparative reactions develop later and are less pronounced. They are manifested by proliferation of endothelial cells and vascular adventitia. The reaction of GNT is bronchial asthma. In the delayed-type hypersensitivity reaction, 2 types of cells are involved - sensitized lymphocytes and macrophages. Lymphocytic and macrophage infiltration in the focus of immune conflict is an expression of chronic immune inflammation in this reaction. The clinical and morphological manifestations of HRT include: tuberculin type reaction, autoimmune diseases, reactions in many viral and some bacterial (viral hepatitis, tuberculosis, brucellosis) infections. Autoimmunization (autoallergy, autoaggression) is a condition characterized by the appearance of reactions of the immune system to normal antigens of one's own tissues. Autoimmune diseases are diseases based on autoimmunity. There are two groups of autoimmune diseases: 1) organ-specific immune diseases that develop due to damage to the physiological barriers of immunologically isolated organs, which allows the immune system to respond to their unchanged antigens by producing autoantibodies and sensitized lymphocytes. At the same time, morphological changes develop in the organs, which are characteristic mainly for HRT. This group includes thyroiditis (Hashimoto's disease), encephalomyelitis, polyneuritis, multiple sclerosis, idiopathic Addison's disease, aspermatogeny, symptomatic ophthalmia; 2) organ-specific autoimmune diseases; leading in these diseases are violations of the control of immunological homeostasis of the lymphoid system. In this case, autoimmunization develops in relation to the antigens of many organs and tissues that do not have organ specificity and are capable of causing the production of antibodies when administered parenterally. In organs and tissues, morphological changes develop that are characteristic of both delayed and immediate types of hypersensitivity reactions. This group of autoimmune diseases includes systemic lupus erythematosus, rheumatoid arthritis, systemic scleroderma, dematomyasitis, secondary thrombotic thrombocytopenic purpura. Immunodeficiency syndromes are extreme manifestations of the insufficiency of the immune system. They can be primary, caused by underdevelopment (hypoplasia, aplasia) of the immune system, - hereditary and congenital, or secondary (acquired), arising in connection with the disease or ongoing treatment. Primary immunodeficiency syndromes can be an expression of insufficiency: cellular and humoral immunity. Combined immunodeficiency states: 1) agammaglobulinemia (hypoplasia of the thymus gland and peripheral lymphoid tissue, lymphopenia, frequent infectious diseases); 2) ataxia, Louis-Barr telangiectasia (hypoplasia of the thymus and peripheral lymphoid tissue, lymphopenia, atrophy of the cerebellar cortex, telangiectasia of the bulbar conjunctiva, mesenchymal malignant tumors, recurrent pneumonia); 3) Nezelof's syndrome (hypoplasia of the thymus and peripheral lymphoid tissue, lymphopenia, sepsis). Cellular immunity deficiency syndrome - Digeorge's syndrome (absence of the thymus and parathyroid glands, absence of T-lymphocytes). Humoral immunity deficiency syndromes: 1) Bruton's syndrome (the thymus gland is preserved, but there are no B-dependent zones and cells of the plasmacytic series in the lymph nodes and spleen; frequent infectious diseases); 2) West's syndrome (the structure of the lymphoid tissue is preserved, frequent infections of the gastrointestinal tract and respiratory tract in combination with autoimmune diseases, allergies). Secondary immunodeficiency syndromes include acquired immune deficiency syndrome or AIDS, an independent disease caused by a specific virus. Other infections, leukemias, malignant lymphomas, thymoma, and sarcoidosis also lead to the development of secondary immunodeficiency syndromes. In these diseases, a deficiency of humoral and cellular immunity occurs as a result of a defect in the population of both B- and T-lymphocytes, and possibly their precursors. Among the types of treatment leading to secondary insufficiency of the immune system, radiation therapy, the use of corticosteroids and immunosuppressants, antilymphocyte serum, thymectomy, and drainage of the thoracic duct are of the greatest importance. LECTURE No. 7. Regeneration. Wound healing Regeneration is the restoration of the structural elements of the tissue to replace the dead. It is a restoration of both structure and function. The factors influencing the course of regeneration include: general (age, intensity of metabolic processes, the state of the hematopoietic and immune systems, etc.) and local (the state of blood vessels, neurotrophic, lymphatic circulation, structural and functional features of organs and tissues, the amount of damage). Regulatory mechanisms of regeneration: 1) humoral factors - keyons, which are glycoproteins and are produced by mature intact cells (epithelial, blood cells, etc.). These substances are released into the blood and inhibit proliferation, increase DNA synthesis and reduce mitotic activity. Antikeylons (mesenchymal factor) are produced in connective tissue (contain proteins and sialic acids); 2) hormonal factors: a) pituitary growth hormone stimulates proliferation and active regeneration; b) mineralocorticoids stimulate, and glucocorticosteroids inhibit the effect on regeneration; c) thyroid hormones stimulate the regeneration process; 3) immune factors - lymphocytes perform an informational role, T-lymphocytes stimulate the healing effect, and B-lymphocytes inhibit; 4) nervous mechanisms of regulation are primarily associated with the trophic function of the nervous system; 5) functional mechanisms - with a functional supply of an organ and (or) tissue. Regeneration phases: 1) proliferation phase - there is an increase in the number of cells or ultrastructures (these are young cambial cells - progenitor cells)); this phase is carried out due to growth factors: platelet, epidermal, fibroblastic, macrophage and lymphocytic; 2) phase of differentiation - young cells mature, their structural and functional specialization occurs. Regeneration classification: 1) according to the level of regeneration: molecular, cellular, subcellular, tissue, organ, systemic; 2) in form: a) cellular regeneration occurs in those organs or tissues (in the epidermis, epithelium of the mucous membranes, endothelium and mesothelium of serous membranes, connective and hematopoietic tissues) where there are labile cells that have a limited lifespan; this form of regeneration is carried out by increasing the number of cells (hyperplasia); b) mixed regeneration occurs in organs and tissues containing stable cells (lungs, liver, kidneys, pancreas, endocrine glands); regeneration is carried out by hyperplasia of the cells themselves, as well as by hyperplasia of ultrastructures inside the cells; if there is a small focus in the liver, then there is a cellular form of regeneration, and with a large damage, regeneration occurs through a combination of ultrastructures and the cells themselves; c) intracellular regeneration occurs exclusively in the ganglion cells of the central nervous system; 3) by types of regeneration - physiological, reparative and pathological. Physiological regeneration is not associated with the action of any damaging factor and is carried out with the help of apoptosis. Apoptosis is a genetically programmed cell death in a living organism. Necrosis is carried out with the participation of hydro- and proteolytic enzymes with the obligatory phenomenon of apoptosis. Apoptosis is carried out due to the activation of calcium-, magnesium-dependent endonucleases, fragmentation of the nucleus and the entire cell occurs. The cell divides into apoptotic bodies. Each fragment contains elements of the nucleus, cytoplasm. This is the phase of formation of apoptotic bodies. Then follows the phase of phagocytosis - apoptotic bodies capture nearby cells and macrophages. No inflammatory reaction occurs. Reparative regeneration occurs when various damaging factors (trauma, inflammation) occur. Complete regeneration, or restitution, is a complete structural and functional restoration; incomplete regeneration, or substitution, occurs in organs with an intracellular form of regeneration and in organs with a mixed form of regeneration, but with extensive damage. In myocardial infarction, the necrosis zone is replaced by connective tissue, along the periphery of the scar, hypertrophy of cardiomyocytes occurs, since ultrastructures and their number increase in them. All this is aimed at restoring functions. The connective tissue is stained green according to Van Gieson, and the scar is red. Pathological regeneration can be excessive (hyperregeneration), delayed (hyporegeneration), metaplasia and dysplasia. Excessive regeneration occurs with a pronounced activation of the first phase of regeneration (bone calluses in fractures, exostoses - bone outgrowths on the plantar surface of the feet, keloid scars, adenoma). Hyporegeneration occurs when the proliferation phase proceeds sluggishly. This occurs in organs and tissues where there is chronic inflammation and where the processes of vascular and nervous trophism are often disturbed (trophic ulcers on the lower extremities, long-term non-healing skin wounds in diabetics, chronic stomach ulcers). Metaplasia occurs in organs and tissues with a cellular form of regeneration, and often it is preceded by chronic inflammation - for example, in smokers and in people with chronic bronchitis, the prismatic epithelium is transformed into a squamous multilayered epithelium with further keratinization. The process can be reversible if you quit smoking and carry out intensive complex treatment; as an unfavorable course - bronchial cancer with the transition to the lung. With anemia and blood diseases, metaplasia of the yellow bone marrow to red occurs. This is a compensatory mechanism. With metaplasia of the connective tissue, it degenerates into cartilaginous, and then into bone. In the gastric mucosa against the background of chronic gastritis, metaplasia occurs when goblet cells appear, which are the precursors of the oncological process. Dysplasia occurs when there is a violation of proliferation and differentiation of cells, therefore, atypical cells appear, i.e., having various shapes and sizes, having large hyperchromic nuclei. Such cells appear among ordinary epithelial cells (in the epithelium of the mucous membrane of the stomach, uterus, intestines). There are three degrees of dysplasia: mild, moderate, severe (when almost all cells of the epithelial layer become atypical and are diagnosed as cancer on the spot). During the regeneration of connective tissue, stage III is distinguished. I. Formation of a young, immature connective - granulation - tissue. It distinguishes between thin-walled blood vessels in large numbers, single leukocytes, macrophages and intermediate substance (proteins, glucose and amino acids). II. The formation of fibrous connective tissue (a large number of fibroblasts, thin collagen fibers and numerous blood vessels of a certain type. III. The formation of scar connective tissue, which contains thick coarse collagen fibers, a small number of cells (fibrocytes) and single blood vessels with thickened sclerotic walls. Wound healing refers to reparative regeneration. There are four types: direct closure of the defect by the creeping epithelium, healing under the scab, healing by primary and secondary intention. Direct closure of an epithelial cover defect is the simplest healing, which consists in the epithelium crawling onto a surface defect and closing it with an epithelial layer. The healing observed on the cornea and mucous membranes under the scab concerns small defects, on the surface of which a drying crust (scab) appears from coagulated blood and lymph; the epidermis is restored under the crust, which disappears on the 3-5th day. Primary intention is the healing of deep wounds with damage not only to the skin, but also to deep-lying tissues; wounds have smooth edges, are not infected and are not contaminated by foreign bodies. On the first day, the wound is cleansed by leukocytes and macrophages, after which the wound defect is filled with granulation tissue, which degenerates into a delicate scar on the 10-15th day. The epithelium creeps on it. Infected, crushed, contaminated and jagged wounds heal by secondary intention; heal through cleansing with leukocytes and macrophages on the 5-6th day. This cleansing is very intense through purulent inflammation - on the 7-8th day, the wound channel is filled with granulation tissue. LECTURE No. 8. Processes of adaptation (adaptation) and compensation The ability of an organism to adapt (adapt) to changing environmental conditions has been developed in the process of phylogenesis and ontogenesis. Adaptation is a general biological process aimed at maintaining the constancy of the internal environment of the body through structural and functional balance. Compensation is a particular manifestation of an adaptation for correcting dysfunctions in case of illness, for saving oneself in a critical situation. Adaptation in pathology can reflect various functional states: functional tension, decrease or perversion of tissue (organ) functions, and therefore can manifest itself in various pathological processes: atrophy, hypertrophy (hyperplasia), organization, tissue restructuring, metaplasia and dysplasia. Atrophy is a life-time decrease in tissue and organ cells in volume, as well as a decrease and even termination of their functions. It occurs both within the normal range and in pathology. During atrophy, apoptosis occurs. Atrophy should be differentiated from similar processes - hypoplasia and aplasia. Hypoplasia is a congenital underdevelopment of an organ that has not reached an extreme degree. Aplasia is a congenital underdevelopment of an organ that has reached an extreme degree, while the organ is an embryonic germ. Types of atrophy: 1) physiological - can be during the development of the organism (evolutionary) and during aging (involutional); so, atrophy of the botallian duct, umbilical cord, urinary duct, thymus (thymus gland) occurs, in the elderly, glands, skin, intervertebral discs, etc. atrophy; 2) pathological - is divided into general and local. General atrophy or cachexia can be the result of various reasons - alimentary with a lack of nutrition, impaired absorption processes in the intestine, etc.; the cause of cancer cachexia is a malignant tumor from the epithelium of the bladder, stomach, esophagus, etc.; pituitary cachexia occurs in the pathology of the pituitary gland (Simmonds disease); cerebral atrophy occurs in the pathology of the hypothalamus. Exhaustion - in other diseases (chronic infections such as tuberculosis, brucellosis, chronic dysentery). Body weight decreases, reserves of adipose tissue decrease, atrophy of internal organs (liver, myocardium, skeletal muscles) occurs. The organs decrease in volume, become more dense on the cut, acquire a brown color. This color is possible due to the fact that lipofuscin accumulates in the cytoplasm (this is a pigment that looks like grains of yellow, orange and brown colors); its grains are located near the mitochondria or even inside them and provide the cell with oxygen. The edge of the liver is sharpened, and the coronary arteries of the heart acquire a tortuous course. Outcome: the process is reversible with timely and comprehensive treatment. An irreversible or pronounced process cannot be treated. Local atrophy can be neurotic (neurotrophic), dysfunctional, a consequence of circulatory failure, pressure, chemical and physical factors. Neurotic atrophy occurs when the connection between organ tissues and the nervous system is disrupted (with nerve damage, with poliomyelitis). Histologically, the preparation is stained according to Van Gieson. In this case, the nerve bundles are depleted, and between them is connective tissue (red) or adipose tissue. Dysfunctional (immobilization) atrophy arises from inactivity during fractures and dislocations. This atrophy is reversible, develops from circulatory failure, due to narrowing of the arteries that feed this organ. Insufficient blood flow causes hypoxia, as a result of which the activity of parenchymal elements decreases, the size of the cells decreases (with vascular atherosclerosis). Atrophy caused by pressure develops even in organs consisting of dense tissue. With prolonged pressure, the integrity of the tissue (usura) is violated, for example, in the vertebral bodies. Emphysema (bloating) of the lungs occurs due to air and an increase in the surface of small bubbles that resemble lung tissue. The lung is compacted, on a cut of a pale gray color, when cut, the tissue crunches (crepites). This is typical for chronic bronchitis, chronic pneumonia, tuberculosis, hereditary emphysema. Outcome: if emphysema is focal, there is no complete change and the cause is lost, then the process is reversible. But in most cases, the process is irreversible. Hydronephrosis occurs when the outflow of urine from the kidneys is impaired. Urine stretches the lumen of the pelvis, compresses the tissue of the kidney, which turns into a bag with thin walls. Causes: stones in the kidneys and ureters; oncological process in the ureters, prostate gland, kidneys; inflammatory process in the prostate gland, urethra. The kidney increases in size. With the onset of hydronephrosis, the process is reversible, but with a long course it is not. Hydrocephalus occurs when there is difficulty in the outflow of cerebrospinal fluid from the ventricles; as a result - their expansion and compression of the brain. Atrophy under the influence of physical and chemical factors. Under the influence of radiation energy, atrophy is especially pronounced in the bone marrow and genital organs. Iodine and thiouracil suppress thyroid function, leading to atrophy. With prolonged use of ACTH, corticosteroids, atrophy of the adrenal cortex and adrenal insufficiency may occur. Hypertrophy (hyperplasia) is an increase in the volume of a cell or tissue due to the multiplication of cells or an increase in their number and size of intracellular ultrastructures. Two types of hypertrophies are adaptive: neurohumoral and hypertrophic growths. Neurohumoral hypertrophy develops on the basis of dysfunction of the endocrine glands, and hypertrophic - as a result of chronic inflammation, in violation of lymph circulation, etc. Organization is the replacement of foci of necrosis of various origins with connective tissue, as well as thrombi, blood clots, fibrinous exudate. A type of organization is encapsulation - the formation of connective tissue around the focus of necrosis or around a foreign body or parasitic animals. Organization stages: 1) cleansing the damaged area from detritus and necrotic tissues with the participation of leukocytes and macrophages; 2) activation of fibroblasts, their synthesis of collagen, as well as lipoaminoglycans; 3) angiomatosis (stage of capillary ingrowth) - blood vessels grow from the perifocal zones into the damaged zone due to endothelial proliferation; 4) granulation tissue, which has blood vessels, passes into fibrous connective tissue and the number of vessels decreases sharply; 5) formation of scar tissue; thanks to lymphoblasts, the scar can shrink, so its elasticity and roughness depend on their number. Tissue restructuring is based on hyperplasia, regeneration and accommodation. For example, collateral circulation, which occurs when blood flow is obstructed in the main vessels. With it, there is an expansion of the lumen of the veins and arteries extending from the affected main vessel, thickening of the walls due to muscle hypertrophy and the formation of elastic fibers. Restructuring in the bones of the spongy substance occurs when the direction of the load changes. Metaplasia is the transition of one type of tissue to another, related to it. It is more common in the epithelium and connective tissue, less often in other tissues. Epidermal or squamous epithelial metaplasia is the transition of prismatic epithelium to keratinizing squamous (in the airways). Protoplasia - the transition of a multilayer non-keratinizing squamous epithelium into a cylindrical one (in the stomach and intestines). Metaplasia of the connective tissue with the formation of cartilage in the bone occurs in scars, the wall of the aorta (with atherosclerosis), in the muscle stroma, in the capsule of healed organs of primary tuberculosis, in the stroma of tumors. Dysplasia is a pronounced violation of the proliferation and differentiation of the epithelium with the development of cellular adaptation and a violation of histoarchitectonics. This is the concept of tissue immunity. Violation of histoarchitectonics in dysplasia is manifested by the loss of the polarity of the epithelium, and sometimes those features that are characteristic of a given tissue or a given organ. There are three stages of dysplasia: mild, moderate and severe. Compensation is a particular type of adaptation; occurs in conditions of pathology in each damaged organ and when its functional tension takes place in the body. Stages of compensation: formation, consolidation and decompensation. At the stage of formation, metabolic processes occur in organs and tissues that are optimal for these conditions. In the fixation stage, hypertrophy occurs in organs and tissues due to hyperplasia of ultrastructures. In the stage of decompensation in hypertrophied tissues there is a deficiency of oxygen, enzymes and a decrease in energy processes. There are two types of compensatory hypertrophy: working, or compensatory (in the heart, gastrointestinal tract, urinary tract), and vicarious, or replacement (observed during death due to illness or after surgery of one of the paired organs). LECTURE No. 9. Sclerosis Sclerosis is a pathological process leading to diffuse or focal compaction of internal organs, vessels, connective tissue structures due to excessive growth of mature dense connective tissue. Moderate sclerosis is called fibrosis. Severe sclerosis is called cirrhosis. Classification There is the following classification of sclerosis. 1. By etiology and pathogenesis: 1) sclerosis as an outcome of chronic productive inflammation of infectious, infectious-allergic and immunopathological genesis, as well as caused by foreign bodies; 2) sclerosis as an outcome of systemic (rheumatic diseases, systemic congenital dysplasia) and local (Dupuytren's contracture, keloid) disorganization of connective tissue; 3) replacement sclerosis as an outcome of tissue necrosis and atrophy as a result of circulatory and metabolic disorders, exposure to physical and chemical factors; 4) formation of scars as a result of wound healing and ulcerative defects; 5) organization of blood clots, hematomas, fibrin deposits, formation of adhesions, obliteration of serous cavities. 2. By morphogenesis: 1) neoplasm of young connective tissue due to the proliferation of fibroblasts, their enhanced synthesis of collagen, fibrillogenesis and the formation of fibrinous scar tissue; 2) increased collagen synthesis by fibroblasts and fibrillogenesis without pronounced cell hyperplasia, a change in the ratio of cells and fibrous structures in favor of the latter, the transformation of loose connective tissue into fibrous tissue, as well as an increase in mass and a change in the structure of specialized types of connective tissue; 3) sclerosis with stromal collapse as a result of necrosis or atrophy of the parenchyma of internal organs. 3. If the reversibility of sclerotic changes is possible, sclerotic processes can be labile or irreversible, stable or partially reversible, progressive or irreversible. Regulation of connective tissue growth in sclerosis is carried out by both central (neuroendocrine) and local (regulatory systems) mechanisms. LECTURE No. 10. Tumors A tumor or neoplasm is a pathological process that occurs in all living organisms. There are more than 200 types of tumors in humans that form in any tissue and in any organ. Malignancy is the transition of tissue into a tumor. Currently, in Russia, lung cancer is the most common among men, followed by stomach and skin cancer. In women - breast cancer, then stomach and skin. Treatment consists primarily of surgery, as well as radiation and chemotherapy. A tumor is a pathological process characterized by the uncontrolled reproduction of cells, while the growth and differentiation of cells are disturbed due to changes in their genetic apparatus. Properties of the tumor: autonomous and uncontrolled growth, atypism, anaplasia or new properties that are not inherent in a normal cell and cataplasia. The structure of the tumor in shape: the shape of the node, mushroom cap, saucer-shaped, in the form of papillae, in the form of cauliflower, etc. Surface: smooth, tuberous, papillary. Localization: in the thickness of the organ, on the surface, in the form of a polyp, diffusely penetrating. On the cut, it can be in the form of a homogeneous white-gray tissue, gray-pink (fish meat), fibrous structure (in the testicles). The size of the tumor depends on the rate and duration of its growth, origin and location. According to the degree of differentiation and growth, the tumor can be: 1) expansive, that is, it grows out of itself, pushing the tissues away. The parenchymal elements surrounding the tumor tissue atrophy, and the tumor is, as it were, surrounded by a capsule. Growth is slower and more often benign. Malignant proceeds in the thyroid gland and kidneys; 2) oppositional growth due to neoplastic transformation of normal cells into tumor cells; 3) infiltrating growth. In this case, the tumor grows into the surrounding tissues and destroys them. Growth occurs in the direction of least resistance (along the interstitial fissures, along the course of nerve fibers, blood and lymphatic vessels). According to the ratio of tumor growth to the lumen of a hollow organ, there are: endophytic (infiltrating growth deep into the organ wall) and exophytic growth (into the organ cavity). microscopic structure. The parenchyma is formed by cells that characterize this type of tumor. The stroma is formed by both the connective tissue of the organ and the cells of the tumor itself. Cells of the tumor parenchyma induce the activity of fibroblasts and can produce the intercellular substance of the stroma. They produce a specific protein substance - angeogenin, under the action of which capillaries are formed in the tumor stroma. Homologous tumors - their structure corresponds to the structure of the organ in which they develop (these are mature differentiated tumors). Heterologous tumors: their cellular structure differs from the organ in which they develop (poorly or undifferentiated tumors). Benign tumors are homologous, slow growing, highly differentiated, do not metastasize and do not affect organization. Malignant tumors consist of little or undifferentiated cells, lose their similarity to tissue, have cellular atypism, grow rapidly and metastasize. Metastases can be hematogenous, lymphogenous, implantation and mixed. In benign tumors, tissue affiliation is easy to determine (unlike malignant ones). It is very important to determine the histogenesis of the tumor, since there are various approaches to treatment. The establishment of tumor histogenesis is based on the function that this tumor cell performs, i.e., it is supposed to determine the substances produced by this cell. It should produce the same substances as normal tissue (for example, a normal fibroblast and a modified by the process of malignancy produce the same substance - collagen). Cell function is also determined by additional staining reactions or by using monoclonal antisera. Tumor histogenesis is sometimes difficult to establish due to the pronounced anaplasia of the cell, which is unable to perform a specific function. If the histogenesis of a malignant tumor cannot be determined, then such a tumor is called blastoma: large cell, spindle cell, polymorphic cell. Blastomas are combined groups of tumors, since various malignant tumors can transform into blastoma. Non-epithelial or mesenchymal tumors develop from connective, adipose, muscle tissue, blood and lymphatic vessels, synovial tissue and bone. 1. Tumors of the connective tissue Connective tissue tumors are: 1) benign - fibromas - can be found wherever there is connective tissue. The most common localization is the dermis. Fibroma is a well-defined node. On the cut, it is fibrous, whitish with a pearly tint. The consistency can be different - from dense elastic to dense. Histology: spindle-shaped tumor cells that fold into bundles running in different directions. The bundles are separated from each other by layers of collagen. The ratio of tumor cells and collagen determines its appearance. There are two types of fibromas: soft fibroma (more tumor cells) and hard (more collagen fibers). Soft fibroma is younger, as it ages, it turns into a hard one; 2) malignant tumors - fibrosarcomas - arise from the elements of the fascia, tendon, from the periosteum. They are localized more often on the limbs, mainly at a young and mature age. Fibrosarcoma is a node without clear boundaries. The tissue of the node on the cut is white with hemorrhages, reminiscent of fish meat (sarcos - fish meat). Histology: 1) the predominance of cells - cellular low-grade fibrosarcoma; 2) the predominance of fibers - fibrous highly differentiated fibrosarcoma; - Slow growth is characteristic, metastases and germination into surrounding tissues are rarely observed. A more favorable prognosis than with poorly differentiated tumors. The tumor is built from spindle-shaped cells, which have foci of cellular polymorphism. To establish the histogenesis of this tumor, a qualitative reaction for collagen (staining according to the Van Gieson method) is used. Intermediate (borderline) tumors are characterized by signs of a benign and malignant tumor: 1) desmoids and fibromatosis (mediastinum, retroperitoneal space); fibromatoses histologically have the structure of a soft fibroma, while they tend to grow into the surrounding tissue, but never give metastases; 2) liposarcomas often occur on the anterior abdominal wall and are mainly found in women; differ: a) highly differentiated liposarcoma; b) myxoid liposarcoma; c) large cell liposarcoma; d) polymorphic cell liposarcoma. Often, signs of all types of liposarcomas are localized in one tumor node. The diagnosis is made after the functions of the tumor cells, i.e. their ability to produce lipids (fat), have been determined. Liposarcoma is characterized by multiple recurrences, as well as late metastases already at the last stage. 2. Bone tumors Bone tumors are: 1) benign - osteoma. It is observed in small bones of the limbs, bones of the skull. It grows in the form of a node (exostosis). Histologically built on the principle of a compact spongy brush, but it differs from normal tissue atypia; 2) malignant - osteosarcoma. The predominant localization is the ends of long tubular bones and metaepiphyseal joints. It occurs mainly at a young age (up to 30 years). Osteosarcoma, one of the most malignant tumors, metastasizes early. Microscopically: tumor osteoblasts of various shapes, areas of osteoplasty (the ability of tumor cells to produce bone tissue). 3. Cartilage tumors Cartilage tumors are: 1) benign - chondroma. Localization in the epiphyses of tubular bones, pelvic bones, femoral head, small bones of the hand; forms: a) echondroma (location on the surface of the bone); b) enchondroma (inside the bone). Depending on this, the volume of surgical intervention is different: in the first case - marginal resection of the bone, in the second - resection of the entire bone with subsequent transplantation. Microscopy: chondrocytes located in the ground substance, a thin connective tissue layer. Any chondroma must be considered as a potentially malignant tumor, since metastases are possible, despite benign growth; 2) malignant - chondrosarcoma. Localization is the same as that of the chondroma. Histology: tumor cells - chondroblasts and foci of chondroplasty (foci of newly formed tumor cartilage). 4. Tumors of vascular tissue Of the arteries, capillaries - angiomas, lymphatic vessels - lymphangiomas. Angiomas are congenital (purple-bluish spots) and acquired. As a result of radiation therapy, congenital angiomas disappear (up to 1 year). After 1 year, fibrosis develops and radiation therapy does not eliminate the tumor. There may be angiomas of the liver, spleen, which are asymptomatic, are detected by chance, are small in size (less than 2 cm). Acquired angiomas are located on the skin, mucous membranes. May appear during pregnancy. Malignant vascular tumors are very rare - hemangioendothelioma. 5. Tumors of muscle tissue Р "Р" Р ° РґРєРёРμ РјС <С С † С < Benign tumors - leiomyomas. Localization: soft tissues of the lower extremities, internal organs (GIT). Most often in the uterus - fibromyoma is a leiomyoma that has undergone fibrosis. Fibromyoma is not so much a tumor as a dyshormonal proliferative process that occurs in women when the balance of sex hormones is disturbed. Malignant: leiomyosarcomas. They are found in the uterus, soft tissues of the extremities. They are characterized by early metastases. РџРѕРїРμСРРμС ‡ РЅРѕ-РїРѕР »РѕСЃР ° С,С <Рμ РјС <С С † С < Tumors of the striated muscle: 1) benign - rhabdomyomas; 2) malignant - rhabdomyosarcomas. One of the most malignant tumors. They are extremely rare. The tumor grows very quickly and leads the patient to death even before the appearance of metastases, as vital organs germinate. Histology: cells - "belts" - elongated cells, sometimes with transverse striation. Cells with a large body and a long process (like a tennis racket). 6. Tumors of hematopoietic tissue Among the tumors of the hematopoietic tissue, there are: 1) leukemia; 2) lymphomas (lymphosarcoma, reticulosarcoma, plasmacytoma or myeloma, lymphogranulomatosis). Tumor tissue contains 2 cellular components: reactive and tumor. The tumor component is giant single-nuclear cells (Hodgkin) and giant multinuclear cells (2 nuclei, in the center of which are Berezovsky-Sternberg cells). These cells are diagnostic. Reactive component: lymphocytes (T and B), plasma cells, eosinophils, leukocytes, macrophages, areas of necrosis resulting from the cytotoxic effect of T-lymphocytes, areas of reactive sclerosis. The reactive and tumor components are found in different ratios, thereby causing a variety of variants of the disease. Lymphocytic predominance The most favorable prognosis. Lymphocytic depletion (tumor predominance). Extreme degree of tumor progression. Intraorganic lesions. The spleen macroscopically takes on the appearance of a village black pudding - dark red in color, with yellow nodes, in a different way - "porphyry spleen" (porphyry is a type of finishing stone). Mixed cellular form (the same ratio of tumor and reactive components). Nodular (ring-shaped) sclerosis The ratio is also equal, but the peculiarity lies in the fact that the connective tissue develops in the form of rings. More often this form is observed in women, and in the initial stage of the disease, the process is localized in the lymph nodes of the mediastinum. Epithelial tumors develop from squamous or glandular epithelium that does not perform any specific function. These are the epidermis, epithelium of the oral cavity, esophagus, endometrium, urinary tract, etc. Benign tumors include papilloma and adenoma. Papilloma is a tumor of squamous or transitional epithelium. It has a spherical shape, dense or soft, with a papillary surface, ranging in size from millet grain to a large pea. It is located above the surface of the skin or mucous membrane on a wide or narrow base. In case of injury, the papilloma is easily destroyed and inflamed, in the bladder it can bleed. After removal of papillomas, in rare cases they recur, sometimes malignant. Adenoma is a tumor of glandular organs and mucous membranes lined with prismatic epithelium. It has the appearance of a well-demarcated node of soft consistency, on the cut the tissue is white-pink, sometimes cysts are found in the tumor. The sizes are different - from a few millimeters to tens of centimeters. Adenomas of the mucous membranes protrude above their surface in the form of a polyp. They are called adenomatous glandular polyps. The adenoma has an organoid structure and consists of cells of prismatic and cubic epithelium. The malignant ones include: 1) cancer in situ is a form of cancer without invasive (infiltrating) growth, but with severe atypism and proliferation of epithelial cells with atypical mitoses; 2) squamous cell (epidermal) cancer develops in the skin and mucous membranes covered with flat or transitional epithelium (oral cavity, esophagus, cervix, vagina). The tumor consists of strands of atypical epithelial cells growing into the underlying tissue, destroying it and forming nested clusters in it. It can be keratinizing (cancer pearls are formed) and non-keratinizing; 3) adenocarcinoma (glandular cancer) develops from the prismatic epithelium of the mucous membranes and epithelium of the glands. The cells are atypical, of various shapes, the nuclei are hyperchromic. Tumor cells form glandular formations of various shapes and sizes, which grow into the surrounding tissue, destroy it, and at the same time their basement membrane is lost; 4) mucous (colloid) cancer - adenogenic carcinoma, the cells of which have signs of both morphological and functional atypia. Cancer cells produce a huge amount of mucus and die in it; 5) solid cancer is an undifferentiated cancer with severe atypia. Cancer cells are located in the idea of trabeculae, separated by layers of connective tissue; 6) fibrous cancer or skirr is a form of undifferentiated cancer, represented by extremely atypical hyperchromic cells located among the layers and strands of coarse fibrous connective tissue; 7) small cell carcinoma is an undifferentiated cancer consisting of monomorphic lymphocyte-like cells that do not form any structures, the stroma is extremely poor; 8) medullary (adenogenic) cancer. Its main feature is the predominance of the parenchyma over the stroma, which is very small. The tumor is soft, white-pink. It is represented by layers of atypical cells, contains many mitoses, grows rapidly and undergoes necrosis early; 9) mixed forms of cancer (dimorphic cancers) consist of the rudiments of two types of epithelium (squamous and cylindrical). LECTURE No. 11. Diseases of the blood Blood diseases develop as a result of dysregulation of hematopoiesis and blood destruction, which is manifested by changes in peripheral blood. Thus, according to the state of peripheral blood indicators, one can say about a malfunction of either the red germ or the white germ. With a change in the red germ, a decrease or increase in the content of hemoglobin and the number of erythrocytes, a violation of the shape of erythrocytes, and a violation of hemoglobin synthesis are observed. Changes in the white germ are manifested by a decrease or increase in the content of leukocytes or platelets. But the analysis of peripheral blood is not always reliable and really reflects the pathological process. The most complete picture of the state of the hematopoietic system is given by the study of bone marrow punctate (sternum) and trepanobiopsy (iliac crest). All blood diseases are divided into anemia, hemoblastosis, thrombocytopenia and thrombocytopathy. 1. Anemia Anemia is a group of diseases characterized by a decrease in the total amount of hemoglobin. In the peripheral blood, erythrocytes of various sizes (poikilocytosis), shapes (anisocytosis), varying degrees of color (hypochromia, hyperchromia), inclusions (basophilic grains, or Jolly bodies, basophilic rings, or Kabo rings) can appear in the peripheral blood. And according to bone puncture, the form of anemia is judged by the state of erythropoiesis (hyper- or hyporegeneration) and by the type of erythropoiesis (erythroblastic, normoblastic and megaloblastic). The reasons for the formation of anemia are different: blood loss, increased blood destruction, insufficient erythropoietic function. Anemia classification By etiology: posthemorrhagic, hemolytic and due to impaired blood formation. By the nature of the course: chronic and acute. According to the state of the bone marrow: regenerative, hyporegenerative, hypoplastic, aplastic and dysplastic. Anemia due to blood loss can be chronic and acute. The pathological anatomy of acute posthemorrhagic anemia is as follows. The cells of the bone marrow of the flat and epiphyses of tubular bones proliferate intensively, the bone marrow becomes juicy and bright. Fatty (yellow) bone marrow of tubular bones also becomes red, rich in erythropoietic and myeloid cells. Foci of extramedullary (extramedullary) hematopoiesis appear in the spleen, lymph nodes, thymus, perivascular tissue, cellular tissue of the renal hilum, mucous and serous membranes, and skin. In chronic posthemorrhagic anemia, the skin and internal organs are pale. Bone marrow of normal flat bones. In the bone marrow of tubular bones, regeneration phenomena expressed to one degree or another and the transformation of fatty bone marrow into red are observed. There is chronic hypoxia of tissues and organs, which explains the development of fatty degeneration of the myocardium, liver, kidneys, degenerative changes in brain cells. There are multiple petechial hemorrhages in the serous and mucous membranes, in the internal organs. Deficiency anemia (due to impaired blood formation), resulting from a lack of iron (iron deficiency), vitamin B12 and folic acid (B12 - deficiency anemia), hypo- and aplastic anemia. Iron deficiency anemia is hypochromic. B12 - deficiency anemia megaloblastic hyperchromic. The skin is pale with a lemon-yellow tint, the sclera is yellow. Hemorrhages form on the skin, mucous membranes and serous membranes. There is hemosiderosis of internal organs, especially the spleen, liver, kidneys. The gastric mucosa is thinned, sclerosed, smooth and devoid of folds. The glands are reduced, their epithelium is atrophic, only the main cells are preserved. Lymphoid follicles are atrophic. Atrophic processes are also present in the intestinal mucosa. The bone marrow of flat bones is raspberry-red, juicy. In tubular bones, the marrow looks like raspberry jelly. In hyperplastic bone marrow, immature forms of erythropoiesis predominate - erythroblasts, which are also found in peripheral blood. The breakdown of myelin and axial cylinders is visualized in the spinal cord. Sometimes foci of ischemia and softening appear in the spinal cord. Hypo- and aplastic anemias are the result of a profound change in hematopoiesis, especially young elements of hematopoiesis. Oppression occurs up to the suppression of hematopoiesis. If only oppression occurs, then young cellular forms of the erythro- and myelopoietic series can be found in the punctate from the sternum. When hematopoiesis is suppressed, the bone marrow is emptied and replaced by fat marrow, thus developing panmyelophthisis. There are multiple hemorrhages in the mucous and serous membranes, phenomena of general hemosiderosis, fatty degeneration of the myocardium, liver, kidneys, ulcerative necrotic processes in the gastrointestinal tract. Hemolytic anemia occurs as a result of the predominance of blood destruction processes over blood formation. They are classified into anemia with intravascular and extravascular hemolysis. Anemias with extravascular hemolysis are divided into erythrocytopathies, erythrocytofermentopathies, and hemioglobinopathies. The pathological picture is as follows. There are general hemosiderosis and suprahepatic jaundice, as well as hemoglobinuric nephrosis. The bone marrow is hyperplastic, pink-red, juicy. In the spleen, lymph nodes, loose connective tissue, foci of extramedullary hematopoiesis appear. 2. Hemoblastosis Hemoblastoses - tumors of the blood system - are divided into two large groups: leukemia (systemic tumor diseases of the hematopoietic tissue) and lymphomas (regional tumor diseases of the hematopoietic or lymphatic tissue). Classification of tumors of hematopoietic and lymphatic tissue There is the following classification. 1. Leukemias (systemic tumor diseases of the hematopoietic tissue): 1) acute leukemia - undifferentiated, myeloid, lymphoblastic, plasmablastic, monoblastic, erythromyeloblastic and megakaryoblastic; 2) chronic leukemia: a) myelocytic origin - myeloid, erythromyeloid leukemia, erythremia, polycythemia vera; b) lymphocytic origin - lymphocytic leukemia, skin lymphomatosis, paraproteinemic leukemia, multiple myeloma, primary macroglobulinemia, heavy chain disease; c) monocytic series - monocytic leukemia and hysteocytosis. 2. Lymphomas (regional tumor diseases of the hematopoietic or lymphatic tissue): 1) lymphosarcoma - lymphocytic, prolymphocytic, lymphoblastic, immunoblastic, lymphoplasmacytic, African; 2) fungal mycosis; 3) Cesari's disease; 4) reticulosarcoma; 5) lymphogranulomatosis (Hodgkin's disease). Leukemia (leukemia) is a progressive overgrowth of leukemia cells. First, they grow in the hematopoietic organs, and then they are hematogenously thrown into other organs and tissues, causing leukemic infiltrates there. Infiltrates can be diffuse (enlarge the affected organ) and focal (tumor nodes are formed that grow into the capsule of the organ and surrounding tissues). It is believed that leukemia is a polyetiological disease, that is, a number of factors favor its formation. There are three main ones: viruses, ionizing radiation and chemicals. The role of viruses in the occurrence of leukemia has been proven by scientific research. This is how retroviruses, the Epstein-Barr virus, work. Ionizing radiation can cause radiation and radiation leukemia, and the frequency of their mutations depends on the dose of ionizing radiation. Among chemicals, the most important are dibenzanthracene, benzopyrene, methylcholanthrene, etc. Acute leukemia is manifested by the appearance of blast cells in the bone marrow, and a leukemia failure in the peripheral blood (a sharp increase in the number of blasts and single mature elements in the absence of transitional forms). A common manifestation for acute leukemia is the presence of an enlarged liver and spleen, the bone marrow of tubular and flat bones is red, juicy, sometimes with a grayish tint. There may be hemorrhages of a different nature in the mucous and serous membranes, organs and tissues, which are complicated by ulcerative necrotic processes and sepsis. A more precise form of leukemia is determined by cytochemical characteristics and cell morphology. Chronic leukemias are such forms of leukemias in which the morphological substrate of tumor growths is more mature than blast blood cells that have reached a certain level of differentiation. Chronic lymphocytic leukemia (CLL) is based on lymphoid hyperplasia and metaplasia of hematopoietic organs (lymph nodes, spleen, bone marrow), accompanied by lymphoid infiltration of other organs and tissues. The tumor nature of CLL is not in doubt, but it is a benign form of the tumor. More often the patient is a man after 40 years. In the punctate of the bone marrow, hyperplasia of lymphoid elements is found, immature forms and bodies of Botkin-Gumprecht increase. There are main clinical and hematological options: 1) classic (generalized enlargement of lymph nodes, spleen, liver, changes in leukemic blood); 2) generalized hyperplasia of peripheral lymph nodes; 3) a variant with a selective increase in one of the groups of lymph nodes; 4) splenomegalic (predominantly enlarged spleen); 5) skin variant - in the form of lymphomas or erythroderma; 6) bone marrow - manifested only by lymphoid metaplasia of the bone marrow. Chronic myeloid leukemia is a systemic blood disease accompanied by myeloid hyperplasia of the bone marrow due to immature granulocytes, the maturation of which is inhibited, myeloid metaplasia of the spleen (dark red with foci of ischemia, sclerosis and hemosiderosis of the pulp), liver (gray-brown with leukemic infiltration along the sinuses , fatty degeneration, hemosiderosis), lymph nodes (grayish-red color with leukemic infiltration) and other organs. The bone marrow of flat bones, epiphyses and diaphyses of tubular bones is gray-red or gray-yellow purulent. Lymphomas are regional tumor diseases of the hematopoietic and lymphatic tissues. Lymphosarcoma is a malignant tumor of lymphocytic cells. Lymph nodes are dense, gray-pink on the cut with areas of necrosis and hemorrhages. The process metastasizes to various organs and tissues. Mycosis fungoides is a relatively benign T-cell lymphoma of the skin. The tumor infiltrate contains plasma cells, histiocytes, eosinophils, and fibroblasts. Nodules of soft consistency, protrude above the surface of the skin, resemble the shape of a fungus, are easily ulcerated and have a blue color. With Sezari's disease, atypical mononuclear cells with sickle-shaped nuclei - Sezari cells - are found in the tumor infiltrate of the skin, bone marrow and blood. Reticulosarcoma is a malignant tumor of reticular cells and histiocytes. Lymphogranulomatosis is a primary neoplastic disease of the lymphatic system. The process occurs unicentrically, spread occurs with the help of metastasis. In 1832, AI Hodgkin examined and described 7 patients with lesions of the lymph nodes and spleen. The disease was called "Hodgkin's disease", which was proposed by S. Wilks in 1865. The etiology is not completely clear. Some believe that lymphogranulomatosis is associated with the Epstein-Barr virus. The genesis of cells (Reed-Berezovsky-Sterner), which are pathognomonic for lymphogranulomatosis, is not clear. These are multinucleated cells that carry antigens on their surface, similar to a lymphoid germ and a monocytoid germ. Pathological anatomy: polymorphocellular granuloma, which consists of lymphocytes, reticular cells, neutrophils, eosinophils, plasma cells and fibrous tissue, is taken as a substrate for lymphogranulomatosis. Lymphogranulomatous tissue initially forms into separate small nodules located inside the lymph node. Further progressing, it displaces the normal tissue of the node and changes its pattern. The histological feature of lymphogranuloma is represented by Berezovsky-Sternberg giant cells. These are large cells with a diameter of 25 microns or more (up to 80 microns), which contain 2 or more round or oval nuclei, often located side by side, which creates the impression of a mirror image. Intranuclear chromatin is delicate, evenly distributed, the nucleolus is clear, large, in most cases eosinophilic. Clinical and morphological classification is shown in Table 1. Table 1 Clinical and morphological classification
With the progression of the disease, lymphocytes disappear from the lesions, which, as a result, is reflected in the change of histological variants, which represent the phases of the development of the disease. The most stable variant is nodular sclerosis. Thrombocytopenia is a group of diseases in which there is a decrease in the number of platelets due to their increased consumption or insufficient formation. Pathological anatomy. The main characteristic is a hemorrhagic syndrome with hemorrhages and bleeding. Hemorrhages occur more often in the skin in the form of petechiae and ecchymosis, less often in the mucous membranes and even more rarely in the internal organs. Bleeding can be both gastric and pulmonary. There may be an increase in the spleen as a result of hyperplasia of its lymphoid tissue, an increase in the number of megakaryocytes in the bone marrow. 3. Thrombocytopathies Thrombocytopathies are a group of diseases and syndromes, which are based on a violation of hemostasis. They are divided into acquired and congenital thrombocytopathies (Chediak-Higashi syndrome, Glanzman's thrombasthenia). Pathological anatomy: manifested as a hemorrhagic syndrome. LECTURE No. 12. Diseases of the cardiovascular system Among the diseases of the cardiovascular system, the most important are: endocarditis, myocarditis, heart defects, cardiosclerosis, atherosclerosis, hypertension, coronary heart disease, cerebrovascular disease and vasculitis. 1. Endocarditis Endocarditis is an inflammation of the endocardium (the inner lining of the heart). There are primary (septic, fibroplastic) and secondary (infectious) endocarditis. Fibroplastic parietal endocarditis with eosinophilia is a rare pathology that manifests itself as severe heart failure, eosinophilic leukocytosis with damage to the skin and internal organs. Pathological anatomy The parietal endocardium of the ventricles of the heart becomes sharply thickened due to fibrosis, elastic fibers are replaced by collagen ones, and thrombotic masses appear on the surface of the endocardium. Skin, myocardium, liver, kidneys, lungs, brain, skeletal muscles, vascular walls and perivascular tissue are infiltrated with cells, among which eosinophils predominate. Thrombosis and thromboembolic complications in the form of heart attacks and hemorrhages are characteristic. The spleen and lymph nodes are enlarged, hyperplasia of the lymphoid tissue with its infiltration by eosinophils. 2. Myocarditis Myocarditis - inflammation of the myocardium, i.e., the muscles of the heart. It can be secondary, due to exposure to viruses, bacteria, rickettsia, etc. As an independent disease, it manifests itself as idiopathic myocarditis, when the inflammatory process occurs only in the myocardium. Pathological anatomy The heart is enlarged, flabby, the cavities are distended. The muscles on the cut are motley, the valves are intact. There are 4 morphological forms: 1) dystrophic, or destructive, type is characterized by hydropic dystrophy and lysis of cardiocytes; 2) the inflammatory-infiltrative type is represented by serous edema and infiltration of the myocardial stroma by various cells - neutrophils, lymphocytes, macrophages, etc.; dystrophic changes are moderately developed; 3) mixed type - a combination of the two types of myocarditis described above; 4) the vascular type is characterized by a predominance of vascular lesions by vasculitis. In other organs, there is congestive plethora, degenerative changes in parenchymal elements, vascular thromboembolism, heart attacks and hemorrhages in the lungs, brain, kidneys, intestines, spleen, etc. 3. Heart disease Heart disease is a persistent, irreversible disorder in the structure of the heart that impairs its function. There are acquired and congenital heart defects, compensated and decompensated. The defect can be isolated and combined. Pathological anatomy Mitral valve disease is manifested by insufficiency or stenosis, or a combination of both. With stenosis, vessels appear in the valve cusps, then the connective tissue of the cusps thickens, they turn into scars, sometimes calcify. Sclerosis and petrification of the fibrous ring are noted. The chords are also sclerosed, becoming thick and shortened. The left atrium expands and its wall thickens, the endocardium becomes sclerosed and becomes whitish. With mitral valve insufficiency, compensatory hypertrophy of the left ventricular wall develops. Aortic valve defect. Fusion of the valve leaflets with each other is noted, lime is deposited in the sclerotic leaflets, which leads to both narrowing and insufficiency. The heart is hypertrophied by the left ventricle. Defects of the tricuspid valve and the valve of the pulmonary artery have the same pathoanatomical picture. 4. Cardiosclerosis Cardiosclerosis is an overgrowth of connective tissue in the heart muscle. There are diffuse and focal (scar after myocardial infarction) cardiosclerosis. Pathologically, focal cardiosclerosis is represented by whitish stripes. Diffuse cardiosclerosis or myofibrosis is characterized by diffuse thickening and coarsening of the myocardial stroma due to the neoplasm of connective tissue in it. 5. Atherosclerosis Atherosclerosis is a chronic disease resulting from a violation of fat and protein metabolism, characterized by damage to the arteries of the elastic and musculo-elastic type in the form of focal deposits in the intima of lipids and proteins and reactive proliferation of connective tissue. Etiology Metabolic (hypercholesterolemia), hormonal (in diabetes mellitus, hypothyroidism), hemodynamic (increased vascular permeability), nervous (stress), vascular (infection, injury) and hereditary factors. Microscopy Microscopically, the following types of atherosclerotic changes are distinguished. 1. Fat spots or stripes are areas of yellow or yellow-gray color that tend to merge. They do not rise above the surface of the intima and contain lipids (stained with Sudan). 2. Fibrous plaques are dense, oval or round, white or white-yellow formations containing lipids and rising above the surface of the intima. They merge with each other, have a bumpy appearance and narrow the vessel. 3. A complication of the lesion occurs when the breakdown of fat-protein complexes predominates in the thickness of the plaque and detritus (atheroma) is formed. The progression of atheromatous changes leads to the destruction of the plaque cover, its ulceration, hemorrhages into the thickness of the plaque and the formation of thrombotic overlays. All this leads to acute blockage of the lumen of the vessel and infarction of the organ supplied by this artery. 4. Calcification or atherocalcinosis is the final stage of atherosclerosis, which is characterized by the deposition of calcium salts into fibrous plaques, i.e., calcification. Petrification of plaques occurs, they become stony. Vessels are deformed. Microscopic examination also determines the stages of atherosclerosis morphogenesis. 1. The prelipid stage is characterized by an increase in the permeability of intimal membranes and mucoid swelling; plasma proteins, fibrinogen, and glycosaminoglycans accumulate. Parietal thrombi are formed, very low density lipoproteins, cholesterol are fixed. Endothelium, collagen and elastic fibers undergo destruction. 2. The lipoid stage is characterized by focal infiltration of the intima with lipids, lipoproteins, and proteins. All this accumulates in smooth muscle cells and macrophages, which are called foam or xanthoma cells. Swelling and destruction of elastic membranes are clearly visualized. 3. Liposclerosis is characterized by the growth of young connective elements of the intima, followed by its maturation and the formation of a fibrous plaque, in which thin-walled vessels appear. 4. Atheromatosis is characterized by the breakdown of lipid masses, which look like a fine-grained amorphous mass with crystals of cholesterol and fatty acids. At the same time, existing vessels can also collapse, which leads to hemorrhage into the thickness of the plaque. 5. The stage of ulceration is characterized by the formation of an atheromatous ulcer. Its edges are undermined and uneven, the bottom is formed by the muscular, and sometimes by the outer layer of the vessel wall. The intimal defect may be covered with thrombotic masses. 6. Atherocalcinosis is characterized by deposition of lime in atheromatous masses. Dense plates are formed - plaque covers. Aspartic and glutamic acids accumulate, with carboxyl groups of which calcium ions bind and precipitate in the form of calcium phosphate. Clinically and morphologically, there are: atherosclerosis of the aorta, coronary and cerebral vessels, atherosclerosis of the arteries of the kidneys, intestines and lower extremities. The outcome is ischemia, necrosis and sclerosis. And with atherosclerosis of the vessels of the intestines and lower extremities, gangrene can develop. 6. Hypertension Hypertension is a chronic disease, the main clinical sign of which is a persistent increase in blood pressure. Classification. By the nature of the course: malignant and benign hypertension. By etiology: primary and secondary hypertension. Clinical and morphological forms: cardiac, cerebral and renal. A number of factors take part in the development mechanism - nervous, reflex, hormonal, renal and hereditary. Pathological anatomy In malignant hypertension, as a result of arteriole spasm, the basement membrane of the endothelium is corrugated and destroyed, its walls are plasma impregnated or fibrinoid necrotic. In benign hypertension, three stages should be distinguished. 1. Preclinical, when the left ventricle is only compensatory hypertrophied. 2. Stage of widespread changes in the arteries. The walls of blood vessels are impregnated with plasma and, as an outcome, hyalinosis or atherosclerosis occurs. Elastofibrosis - hypertrophy and splitting of the internal elastic membrane and proliferation of connective tissue. 3. Secondary changes in organs develop in two ways: either slowly, leading to atrophy of the parenchyma and sclerosis of organs, or at lightning speed - in the form of hemorrhages or heart attacks. 7. Ischemic heart disease Ischemic heart disease is a group of diseases caused by absolute or relative insufficiency of coronary blood flow. The immediate causes are prolonged spasm, thrombosis, atherosclerotic occlusion, as well as psycho-emotional overstrain. The pathogenetic factors of coronary disease are the same as in atherosclerosis and hypertension. The course is undulating with short crises, against the background of chronic insufficiency of the coronary circulation. Myocardial infarction is ischemic necrosis of the heart muscle. Classification By the time of occurrence: acute (first hours), acute (2-3 weeks), subacute (3-8 weeks) and scarring stage. By localization: in the basin of the anterior interventricular branch of the left coronary artery, in the basin of the circumflex branch of the left coronary artery and the main trunk of the left coronary artery. According to the localization of the necrosis zone: anteroseptal, anteroapical, anterolateral, high anterior, widespread anterior, posterior diaphragmatic, posterobasal, posterolateral and widespread posterior. By prevalence: small-focal, large-focal and transmural. Downstream: necrotic stage and scarring stage. In the necrotic stage (histologically), the infarction is a zone of necrosis in which islets of preserved myocardium are preserved perivascularly. The zone of necrosis is separated from healthy tissue by a demarcation line (leukocyte infiltration). The stage of scarring is said when macrophages and young cells of the fibroplastic series take the place of leukocytes. The newly formed connective tissue is loose at first, then it matures and turns into coarse fibrous tissue. Thus, when organizing a heart attack, a dense scar is formed in its place. 8. Cerebrovascular disorders Cerebrovascular diseases are diseases that occur as a result of an acute violation of cerebral circulation. The background is hypertension and atherosclerosis. Distinguish between transient ischemic attack and stroke. Stroke can be hemorrhagic or ischemic. In transient ischemic attack, the changes are reversible. At the site of small hemorrhages, perivascular deposits of hemosiderin can be determined. In a hemorrhagic stroke, a brain hematoma is formed. At the site of the hemorrhage, the brain tissue is destroyed, a cavity is formed filled with blood clots and softened brain tissue (red softening of the brain). The cyst has rusty walls and brownish contents. In ischemic stroke, a focus of gray softening is formed. 9. Vasculitis Vasculitis is a disease characterized by inflammation and necrosis of the vascular wall. There are local (transition of the inflammatory process to the vascular wall from the surrounding tissues) and systemic vasculitis. Classification According to the type of inflammatory reaction, they are divided into necrotic, destructive-productive and granulomatous. According to the depth of the lesion of the vascular wall, they are divided into endovasculitis, mesovasculitis and perivasculitis, and when combined, into endomesovasculitis and panvasculitis. By etiology: secondary and primary vasculitis. Primary vasculitis is divided depending on the caliber of the vessel into: 1) predominant damage to the aorta and its large branches (nonspecific aortoarteritis - Takayasu's disease, temporal arteritis - Horton's disease); 2) damage to small and medium-sized arteries (nodular periarteritis, allergic granulomatosis, systemic necrotizing vasculitis, Wegener's granulomatosis, lymphatic syndrome with lesions of the skin and mucous membranes); 3) damage to small-caliber arteries (thrombangitis obliterans - Buerger's disease); 4) damage to arteries of various calibers (mixed unclassified form). Secondary vasculitis is classified by etiological agent: 1) with infectious diseases (syphilitic, tuberculous, rickettsial, septic, etc.); 2) with systemic connective tissue diseases (rheumatic, rheumatoid and lupus); 3) hypersensitivity vasculitis (serum sickness, Henoch-Schonlein purpura, essential mixed cryoglobulinemia, malignant neoplasms). Due to the development of vasculitis in organs and tissues, the following changes occur - heart attacks, post-infarction large-focal and small-focal sclerosis, atrophy of parenchymal elements, gangrene and hemorrhages. A common pathological picture for all vasculitis is inflammatory processes in all vessels, followed by sclerosis or necrosis. LECTURE No. 13. Diseases of the respiratory system Among respiratory diseases, acute bronchitis, acute inflammatory and destructive lung diseases, chronic nonspecific lung diseases, bronchial and lung cancer, and pleurisy are of the greatest importance. 1. Acute bronchitis Acute bronchitis is an acute inflammation of the bronchial tree. Etiology: viruses and bacteria. Predisposing factors are hypothermia, chemical factors and dust, as well as the general state of the immune system. Pathological anatomy. The mucous membrane of the bronchi becomes full-blooded and swells. Small hemorrhages and ulcerations are possible. There is a lot of mucus in the lumen of the bronchi. In the mucous membrane, various forms of catarrh develop (serous, mucous, purulent and mixed), fibrous and fibrous-hemorrhagic inflammation. Possible destruction of the bronchus with ulceration in the mucous membrane (destructive-ulcerative bronchitis). The thickening of the bronchial wall is due to its infiltration by lymphocytes, macrophages, plasma cells and proliferation of the endothelium. The outcome depends on the depth of the lesion of the bronchus wall. The deeper, the lower the percentage of regeneration; the outcome also depends on the type of catarrh and the length of stay of the pathogen. 2. Acute inflammatory diseases of the lungs (pneumonia) There are primary and secondary pneumonia (as complications of many diseases). Primary pneumonia is divided into interstitial, parenchymal and bronchopneumonia, secondary pneumonia - into aspiration, hypostatic, postoperative, septic and immunodeficiency. According to the prevalence of pneumonia, they are divided into miliary, acinous, lobular, confluent, segmental, polysegmental and lobar. By the nature of the inflammatory process, pneumonia can be serous, serous-leukocytic, serous-desquamative, serous-hemorrhagic, purulent, fibrinous and hemorrhagic. Croupous pneumonia Croupous pneumonia is an acute infectious-allergic disease. Pathologically, 4 stages are distinguished: 1) the stage of the tide lasts a day and is characterized by a sharp hyperemia, microbial edema of the affected lobe, and the permeability of the vascular wall increases. First, diapedetic impregnation occurs in the lumen of the alveoli. The lung is compacted and full-blooded; 2) the stage of red hepatization is formed on the 2nd day of the disease. Diapedesis of erythrocytes intensifies, neutrophils join them and fibrin strands fall out. A large amount of pathogen; the lymphatic vessels are overflowing with lymph, the lung tissue becomes dense and acquires a dark red color. Regional lymph nodes are enlarged and plethoric; 3) the stage of gray hepatization occurs on the 4-6th day of the disease. In the lumen of the alveoli, fibrin and neutrophils accumulate, which, together with macrophages, phagocytize bacteria. Erythrocytes undergo hemolysis. The lung becomes gray and compacted. The lymph nodes of the root of the lung are white-pink and enlarged; 4) the stage of resolution occurs on the 9-11th day of the disease. Fibrinous exudate under the influence of proteolytic enzymes and macrophages undergoes melting and resorption, and then is excreted through the lymphatic drainage of the lung and through sputum. Common manifestations of lobar pneumonia include dystrophic changes in parenchymal organs, their plethora, hyperplasia of the spleen and bone marrow, plethora and cerebral edema. Bronchopneumonia Bronchopneumonia is an inflammation of the lungs that develops against the background of bronchitis or bronchiolitis. It can be focal (primary) and common (secondary) - as a complication of many diseases. Unlike lobar pneumonia, bronchopneumonia is always accompanied by an inflammatory process in the bronchi. As a rule, the exudate is distributed unevenly, and the interalveolar septa are permeated with cellular infiltrate. Interstitial (interstitial) pneumonia is characterized by the development of an inflammatory process in the stroma of the lung. The cause of this pneumonia can be viruses, pyogenic bacteria and fungi. There are three types of interstitial pneumonia. 1. Peribronchial pneumonia - occurs when the inflammatory process begins in the wall of the bronchus, passes to the peribronchial tissue and spreads to the adjacent interalveolar septa. The walls of the partitions thicken. Macrophages and single neutrophils accumulate in the alveoli. 2. Interlobular pneumonia - occurs when the inflammatory process spreads to the interlobular septa from the side of the lung tissue, visceral pleura and mediastinal pleura. When the process takes on a phlegmonous character, the lung is stratified into lobules - there is a stratifying or sequestering interstitial pneumonia. 3. Interalveolar pneumonia is a morphology of interstitial lung disease. 3. Acute destructive processes in the lungs Abscess An abscess is a cavity filled with inflammatory exudate. Lung abscess can be pneumogenic in nature, then first there is necrosis of the lung tissue and its purulent fusion. The molten purulent-necrotic mass is excreted through the bronchi with sputum, a cavity is formed. With the bronchogenic nature of the abscess, the bronchus wall is first destroyed, followed by a transition to the lung tissue. The wall of the abscess is formed by both bronchiectasis and compacted lung tissue. Gangrene Pulmonary gangrene is characterized as a severe outcome of any inflammatory process in the lungs. The lung tissue undergoes wet necrosis, becomes grey-dirty and has a fetid odor. 4. Chronic nonspecific lung diseases The mechanism of their development is different. Bronchogenic - is a violation of the drainage function of the lungs and leads to a group of diseases called chronic obstructive pulmonary disease. The pneumogenic mechanism leads to chronic non-obstructive lung disease. The pneumonitogenic mechanism leads to chronic interstitial lung disease. Chronical bronchitis Chronic bronchitis is a prolonged acute bronchitis. The microscopic picture is varied. In some cases, the phenomena of chronic mucous or purulent catarrh with increasing atrophy of the mucous membrane, cystic transformation of the glands, metaplasia of the integumentary prismatic epithelium into stratified squamous epithelium, and an increase in the number of goblet cells predominate. In other cases, in the wall of the bronchus and especially in the mucous membrane, cellular inflammatory infiltration and proliferation of granulation tissue are pronounced, which swells in the lumen of the bronchus in the form of a polyp (polypous bronchitis). When granulation tissue matures and connective tissue grows into the walls of the bronchus, the muscle layer atrophies, and the bronchi become deformed (deforming chronic bronchitis). bronchiectasis Bronchiectasis is an expansion of the bronchi in the form of a cylinder or bag, which can be congenital or acquired, single or multiple. Microscopically: the bronchiectasis cavity is lined with prismatic or stratified epithelium. In the wall of bronchiectasis, there are signs of chronic inflammation. Elastic and muscle fibers are replaced by connective tissue. The cavity is filled with pus. The lung tissue that surrounds bronchiectasis is dramatically altered. Abscesses and fields of fibrosis appear in it. Sclerosis develops in the vessels. With multiple bronchiectasis, hyperplasia occurs in the pulmonary circulation and hypertrophy of the right ventricle of the heart. Thus, the formation of a cor pulmonale occurs. Emphysema Emphysema is a pathological condition characterized by excessive air content in the lungs and an increase in their size. There are 6 types of emphysema. 1. Chronic diffuse obstructive pulmonary emphysema. The cause is usually chronic bronchitis or bronchiolitis. Macroscopically: the lungs are enlarged in size, cover the anterior mediastinum with their edges, swollen, pale, soft, do not fall down and are cut with a crunch. The walls of the bronchi are thickened, in their lumen there is a mucopurulent exudate. Microscopically: the bronchial mucosa is full-blooded, with the presence of an inflammatory infiltrate and a large number of goblet cells. There is an expansion of the wall of the acini. If they are completely expanded, then panacinar emphysema occurs, and if only the proximal sections are expanded, central emphysema. Stretching of the acini leads to stretching and thinning of elastic fibers, expansion of the alveolar ducts, and changes in the alveolar septa. The walls of the alveoli become thinner and straighten, the interalveolar septa expand, and the capillaries become empty. Thus, the bronchioles expand, the alveolar sacs shorten, and collagen fibers grow in the interalveolar capillaries (intracapillary sclerosis). There is an alveolar-capillary block, which leads to hypertension of the pulmonary circulation and the formation of a cor pulmonale. 2. Chronic focal emphysema, or perifocal cicatricial emphysema. All of the above pathological changes occur in the local area of the lungs. As a rule, this is preceded by a tuberculous process or the presence of postinfarction scars. Hypertrophy of the pulmonary circulation is not typical. 3. Vicarious (compensatory) emphysema occurs after removal of a part or lobe of the lung. There are hypertrophy and hyperplasia of the structural elements of the lung tissue. 4. Primary (idiopathic) panacytic emphysema is morphologically represented by atrophy of the alveolar wall, reduction of the capillary wall and severe hypertension of the pulmonary circulation. 5. Senile emphysema pathologically manifests itself as obstructive, but occurs as a result of physiological aging of the body. 6. Interstitial emphysema differs from others in the occurrence of ruptures in the alveoli and the entry of air into the interstitial tissue, and then spreads to the mediastinum and subcutaneous tissue of the neck. Bronchial asthma Bronchial asthma is a disease characterized by attacks of expiratory dyspnea, which occur as a result of impaired bronchial patency. The causes of this disease are allergens or infectious agents, or a combination of both. We should not forget about drugs that, acting on β-receptors, can cause bronchial obstruction. These drugs include a group of β-blockers. Pathological anatomy in the lungs in asthma can be different. So, in the acute period (during an attack), there is a sharp plethora of vessels of the microcirculatory bed and an increase in their permeability. Edema of the mucous and submucosal layers develops. They are infiltrated by mastocytes, basophils, eosinophils, lymphoid and plasma cells. The basement membrane of the bronchi thickens and swells. There is hypersecretion of mucus due to goblet cells and mucous glands. In the lumen of the bronchi accumulates a mucous secret with an admixture of eosinophils and cells of the desquamated epithelium, which prevents the passage of air. If an allergic reaction occurs, then an immunohistochemical study reveals the luminescence of IgE on the surface of the cells. With repeated attacks, diffuse chronic inflammation, thickening and hyalinosis of the basement membrane, sclerosis of the interalveolar septa and chronic obstructive pulmonary emphysema develop in the bronchial wall. Hypertension of the pulmonary circulation occurs, which leads to the formation of a cor pulmonale and, as a result, to cardiopulmonary insufficiency. chronic abscess Along the outflow of lymph from the wall of a chronic abscess to the root of the lung, whitish layers of connective tissue appear, which leads to fibrosis and deformation of the lung tissue. chronic pneumonia In this disease, areas of carnification and fibrosis are combined with cavities of chronic pneumoniogenic abscesses. Chronic inflammation and fibrosis develop along the lymphatic vessels, in the interlobular septa, and in the perivascular and peribronchial tissue, resulting in pulmonary emphysema. In the vascular wall of small and medium caliber, inflammatory and sclerotic processes appear, up to their obliteration. As a rule, bronchiectasis and foci of inflammation are formed, which later sclerosis and deform the lung tissue. Interstitial lung diseases include a group of diseases characterized by a primary inflammatory process in the interalveolar pulmonary interstitium. Morphologically, there are three stages. In the stage of alveolitis, there is an increasing diffuse infiltration of the interstitium of the alveoli, alveolar ducts, the walls of the respiratory and terminal bronchioles with neutrophils, lymphocytes, macrophages, and plasma cells - this is what diffuse alveolitis looks like. In granulomatous alveolitis, the process is local in nature and is characterized by the formation of macrophage granules both in the interstitium and in the vessel wall. Cellular infiltration leads to thickening of the alveolar interstitium, capillary compression, and hypoxia. The stage of disorganization of the alveolar structures and pneumofibrosis is manifested by deep damage to the alveolar structures. Endothelial and epithelial membranes and elastic fibers are destroyed, cell infiltration of the alveolar interstitium increases and collagen fibers are formed, diffuse pneumosclerosis develops. At the stage of formation of a honeycomb lung, panacic emphysema develops, bronchiectasis occurs, and cysts with fibrously altered walls appear in place of the alveoli. pneumofibrosis Pneumofibrosis is a pathological condition manifested by the growth of connective tissue in the lung. Pneumofibrosis completes the development of various processes in the lungs. In other words, the entire bronchopulmonary system is replaced by connective tissue, which leads to lung deformation. Lung cancer There is the following classification of lung cancer. 1. By localization: 1) radical (central), which comes from the stem, lobar and initial part of the segmental bronchus; 2) peripheral, coming from the peripheral section of the segmental bronchus and its branches, as well as from the alveolar epithelium; 3) mixed. 2. By the nature of growth: 1) exophytic (endobronchial); 2) endophytic (exobronchial and peribronchial). 3. By microscopic form: 1) plaque-like; 2) polyposis; 3) endobronchial diffuse; 4) knotty; 5) branched; 6) knotty-branched. 4. By microscopic appearance: 1) squamous (epidermoid); 2) adenocarcinoma, undifferentiated anaplastic cancer (small and large cell); 3) glandular squamous cell carcinoma; 4) carcinoma of the bronchial glands (adenoid cystic and mucoepidermal). Radical cancer develops in the mucous membrane of the stem, lobar and initial parts of the bronchial segment. Initially, a plaque is formed, and later, depending on the nature of growth, it acquires a microscopic form. Radical cancer often has a structure of a squamous type than other types. Peripheral cancer often has a glandular appearance and develops from the alveolar epithelium, so it is painless and is detected incidentally during routine examinations or when it moves to the pleura. Highly differentiated squamous cell epidermal carcinoma is characterized by the formation of keratin by many cells and the formation of cancerous pearls. Moderately differentiated cancer is characterized by mitosis and cell polymorphism. Poorly differentiated cancer is manifested by even greater cell polymorphism, a large number of mitoses, keratin is determined only in individual cells. In well-differentiated adenocarcinoma, cells in the acinar, tubular, or papillary structures produce mucus. Moderately differentiated adenocarcinoma has a glandular-soloid structure, it contains a large number of mitoses. Poorly differentiated consists of solid structures, and its polygonal cells produce mucus. Undifferentiated anaplastic lung cancer can be small cell or large cell. Small cell carcinoma consists of small lymphoid or oat-shaped cells with a hyperchromic nucleus, the cells grow in sheets or strands. Large cell carcinoma is represented by large polymorphic and multinucleated cells that produce mucus. Glandular squamous cell lung cancer is a mixed cancer, as it is a combination of adenocarcinoma and squamous cell carcinoma. Pleurisy Pleurisy is inflammation of the pleura. The etiology can be very diverse - for example, with toxic or allergic pleurisy, the visceral pleura becomes dull with the presence of pinpoint hemorrhages. Sometimes it is covered with fibrous overlays. With pleurisy, serous, serous-fibrinous, fibrinous, purulent or hemorrhagic exudate accumulates in the pleural cavity. When there are fibrinous overlays on the pleura and there is no effusion, they speak of dry pleurisy. The accumulation of purulent exudate is called pleural empyema. LECTURE No. 14. Diseases of the gastrointestinal tract 1. Diseases of the esophagus The most common diseases are diverticula, inflammation and tumors. Esophageal diverticulum A diverticulum of the esophagus is a limited blind protrusion of its wall, which may consist of all layers of the esophagus (true diverticulum) or only the mucous and submucosal layers (muscular diverticulum). esophagitis Esophagitis is an inflammation of the lining of the esophagus. There are chronic and acute esophagitis. Acute can be catarrhal, fibrinous, phlegmonous, ulcerative and gangrenous. Chronic esophagitis is manifested by hyperemia and edema of the mucous membrane, with areas of epithelial destruction, leukoplakia and sclerosis. Esophageal carcinoma Esophageal cancer is more often localized on the border of the middle and lower third of its duration. The following microscopic forms are distinguished: ring-shaped dense, papillary and ulcerated. Ring-shaped dense cancer is a tumor formation that circulatory covers the wall of the esophagus in a certain area. Papillary cancer of the esophagus easily disintegrates, and ulcers are formed that can penetrate into neighboring organs and tissues. Ulcerated cancer is a cancerous ulcer that is oval in shape and extends along the esophagus. Microscopically, the following forms of esophageal cancer are distinguished: carcinoma in situ, squamous cell carcinoma, adenocarcinoma, squamous glandular, glandular cystic, mucoepidermal and undifferentiated cancer. 2. Diseases of the stomach The most common are gastritis, peptic ulcer and cancer. Gastritis Gastritis is an inflammation of the lining of the stomach. There are acute and chronic gastritis. In acute gastritis, inflammation can cover the entire stomach (diffuse gastritis) or certain parts of it (focal gastritis). The latter is divided into fundic, antral, pyloroantral and pyloroduodenal gastritis. Depending on the characteristics of morphological changes in the gastric mucosa, the following forms of acute gastritis are distinguished: 1) catarrhal, or simple; 2) fibrinous; 3) purulent (phlegmous); 4) necrotic. With catarrhal gastritis, the gastric mucosa is thickened, edematous, hyperemic, its surface is abundantly covered with mucous masses, multiple small hemorrhages and erosion are visible. Microscopically revealed dystrophy, necrobiosis and desquamation of the surface epithelium. The glands change slightly. The mucous membrane is permeated with serous, serous-mucous or serous-leukocytic exudate, and its own layer is full-blooded and edematous, infiltrated with neutrophils. With fibrinous gastritis, a fibrinous film of gray or yellow-brown color is formed on the surface of the thickened mucous membrane. According to the depth of penetration, necrosis can be superficial (croupous) and deep (diphtheritic). With purulent gastritis, the wall of the stomach becomes sharply thickened, the folds are coarse, with the presence of hemorrhages and fibrinous-purulent overlays. Necrotizing gastritis usually occurs with a chemical burn of the stomach. Necrosis can cover the superficial or deep sections of the mucosa and differs in coagulation and colliquation. Chronic gastritis can be autoimmune (type A gastritis) or non-immune (type B gastritis). With autoimmune gastritis, the formation of antibodies to parietal cells occurs, so the fundus is more often affected. In connection with the defeat of the parietal cells, the production of hydrochloric acid is reduced. With non-immune gastritis, the antrum is affected and the production of hydrochloric acid is moderately reduced. Topographically distinguish antral, fundal and pangastritis. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane, as a result of which there is a violation of its regeneration and structural restructuring of the mucous membrane. Peptic ulcer disease Peptic ulcer is a chronic relapsing disease, morphologically expressed by the formation of gastric or duodenal ulcers. According to localization, ulcers located in the pyloroduodenal zone or the body of the stomach are distinguished, although there are also combined forms. The reasons for the formation of ulcers are different: the infectious process, allergic, toxic and stress factors, drug and endocrine factors, as well as postoperative complications (peptic ulcers). It is important to note the presence of predisposing factors - this is senile age, male sex, the first blood group, etc. During the formation of an ulcer, an important role is played by erosion, which is a defect in the mucous membrane that does not penetrate beyond the muscle layer. Erosion is formed as a result of necrosis of the mucous membrane area, followed by hemorrhage and rejection of dead tissue. At the bottom of the erosion there is hydrochloric hematin, and in its edges there is a leukocyte infiltrate. Erosion is easily epithelialized, but with the development of peptic ulcer, some erosions do not heal, deep layers of the stomach wall begin to undergo necrosis. An acute ulcer has an irregular round or oval shape and resembles a funnel. As the necrotic masses are cleared, the bottom of the acute ulcer, represented by the muscular layer, is revealed. The bottom is painted (due to hematin) in a dirty gray or black color. A chronic ulcer has a clear oval or round shape, ranging in size from a few millimeters to 5-6 cm, penetrates into the stomach wall at various depths, up to the serous layer. The bottom of the ulcer is smooth, sometimes rough, the edges are rolled up and dense. The edge of the ulcer facing the esophagus is undermined, and the mucous membrane hangs over it, and the opposite edge is flat. There is a period of remission and exacerbation. During the period of remission, there is scar tissue at the edges of the ulcer, the mucous membrane along the edges is thickened and hyperemic. In the bottom area, there is a destroyed muscle layer, which is replaced by scar tissue, in which there are many vessels with thickened walls. Nerve fibers and ganglion cells undergo dystrophic changes and decay. During the period of exacerbation, a wide zone of fibrinoid necrosis appears in the area of the bottom and edges of the ulcer. On the surface of necrotic masses is located fibrinous-purulent or purulent exudate. The zone of necrosis is limited by granulation tissue with a large number of thin-walled vessels and cells, among which there are many eosinophils. Below is coarse fibrous scar tissue. Stomach cancer There is the following classification of stomach cancer. 1. By localization, they distinguish: pyloric, lesser curvature of the body with a transition to the walls, cardiac, greater curvature, fundic and total. 2. According to the nature of growth, three forms are distinguished: 1) with predominantly exophytic growth (plaque-like, polypous, fungous, or mushroom-like, and ulcerated); 2) with predominantly endophytic infiltrating growth (infiltrative-ulcerative, diffuse); 3) with exoendophytic growth, or mixed. 3. Adenocarcinoma (tubular, papillary, mucinous), undifferentiated (solid, scirrhous, parietal), squamous, glandular-squamous (adenocancroid) and unclassified cancer are isolated microscopically. Pathological anatomy. Plaque cancer affects the submucosal layer. Polyposis cancer is gray-pink or gray-red in color and rich in blood vessels. These two forms of cancer histologically have the structure of adenocarcinoma or undifferentiated cancer. Fungal cancer is a nodular formation with erosions on the surface, as well as hemorrhages or fibrinous-purulent overlays. The swelling is soft, grey-pink or grey-red and well circumscribed; Histologically, it appears to be adenocarcinoma. Ulcerated cancer by genesis is a malignant tumor, it is represented by primary ulcerative, saucer-shaped cancer and cancer from a chronic ulcer (ulcer-cancer). Primary ulcerative cancer is microscopically represented by undifferentiated cancer. Saucer cancer is a round formation, reaching a large size, with roller-like whitish edges and ulceration in the center. The bottom of the ulcer can be represented by other (adjacent) organs. Histologically it is represented by adenocarcinoma. Ulcer-cancer is characterized by the formation of an ulcer at the site and is manifested by the growth of scar tissue, sclerosis and thrombosis of blood vessels, destruction of the muscle layer at the bottom of the ulcer and thickening of the mucous membrane around the ulcer. Histologically, it looks like adenocarcinoma, less often undifferentiated cancer. Infiltrative-ulcerative carcinoma is characterized by severe cancrotic infiltration of the wall and ulceration of the tumor, and histologically it is represented by adenocarcinoma or undifferentiated cancer. Diffuse cancer is manifested by thickening of the stomach wall, the tumor is dense, whitish and immobile. The mucous membrane has an uneven surface, and folds of uneven thickness with erosions. Defeats can be limited and total. As the tumor grows, the stomach wall shrinks. Histologically, cancer is an undifferentiated form of carcinoma. Transitional forms have different clinical and morphological forms. 3. Bowel disease Enteritis Enteritis, or inflammation of the small intestine: according to localization, inflammation of the duodenum (duodenitis), jejunum (eunit) and ileum (ileitis) are distinguished. Enteritis can be chronic and acute. Acute enteritis histologically can be catarrhal, fibrinous, purulent and necrotic-ulcerative. With catarrhal enteritis, the mucous membrane is plethoric, edematous, covered with serous, serous-mucous or serous-purulent exudate. The inflammatory process also covers the submucosal layer. The epithelium undergoes dystrophy and desquamation, goblet cells are hyperplastic, minor erosions and hemorrhages are noted. With fibrous enteritis, the mucous membrane is necrotic and permeated with fibrinous exudate, gray or gray-brown overlays on the surface. Depending on the depth of necrosis, inflammation can be croupous and diphtheritic, with rejection of the latter, deep ulcers form. With purulent enteritis, the walls of the intestine are saturated with pus or pustules are formed. With necrotic-ulcerative enteritis, destructive processes occur in the group and solitary lymphatic follicles of the intestine or in the mucous membrane without connection with the lymphatic apparatus. With any kind of process, hyperplasia and reticulomacrophage transformation of the intestinal lymphatic apparatus develop. In chronic enteritis, two forms are distinguished - without atrophy of the mucous membrane and atrophic enteritis. For enteritis without atrophy of the mucous membrane, uneven thickness of the villi and the appearance of club-shaped thickenings of their distal parts are characteristic. The cytoplasm of villi enterocytes is vacuolated. Adhesions appear between the enterocytes of the apical parts of the adjacent villi, the stroma of the villi is infiltrated with plasma cells, lymphocytes, and eosinophils. The cellular infiltrate descends from the crypt, which may be cystically dilated. The infiltrate pushes the crypts apart and reaches the muscular layer of the mucous membrane. With atrophy, the villi shorten, grow together and deform - they collapse argyrophilic fibers. Enterocytes are vacuolated. A large number of goblet cells appear. The crypts are atrophied or cystically dilated, and also infiltrated with lymphohistiocytic elements and replaced by outgrowths of collagen and muscle fibers. If atrophic processes occur only in the villi, then this is a hyperregenerative variant of atrophy, and if both villi and crypts are atrophic, then there is a hyporegenerative variant of atrophy. Enteropathy Enteropathy is a chronic disease of the small intestine, which is based on hereditary and acquired enzymatic disorders of enterocytes. Enteropathies include: 1) disaccharidosis deficiency; 2) hypercatabolic hypoproteinemic enteropathy; 3) gluten enteropathy. Pathological anatomy. There are various degrees of severity of dystrophic and atrophic changes. The villi shorten and thicken, the number of enterocytes decreases, they vacuolize and lose microvilli. The crypts deepen and the membrane thickens, and the mucosa is infiltrated by plasma cells, lymphocytes, and macrophages. In later periods, the villi are absent, and there is a sharp sclerosis of the mucous membrane. With hypercatabolic hypoproteinemic enteropathy (in combination with the pathological anatomical picture described above), there is a sharp expansion of the lymphatic capillaries and vessels of the intestinal wall. Histoenzymatic study of biopsy specimens of the intestinal mucosa allows you to determine enzyme disorders for a certain type of enteropathy. Colitis Colitis is an inflammation of the large intestine. With the defeat of the predominantly blind section, they speak of typhlitis, the transverse colon section - about transverse, the sigmoid - about sigmoiditis and the rectum - about proctitis. Inflammation of the entire colon is called pancolitis. Inflammation can be chronic or acute. Acute colitis has 7 forms. Catarrhal colitis is manifested by hyperemia and swelling of the mucous membrane, and on its surface there is a serous, mucous or purulent exudate. The inflammatory infiltrate permeates the entire mucosal and submucosal layers, and hemorrhages are visualized. Degeneration and necrobiosis of the epithelium are combined with desquamation of the surface epithelium and hypersecretion of the glands. Fibrinous colitis, depending on the depth of necrosis of the mucous membrane and the penetration of fibrinous exudate, can be croupous and diphtheritic. Purulent colitis is characterized by phlegmonous inflammation. With hemorrhagic colitis, multiple hemorrhages occur in the intestinal wall, and it is saturated with blood. With necrotizing colitis, not only the mucous layer, but also the submucosal layer undergoes necrosis. Gangrenous colitis is a variant of necrotizing colitis. With ulcerative colitis, ulcers form in the intestinal mucosa, and, as a result, dystrophic or necrotic changes in the intestinal wall occur. Chronic colitis is without atrophy of the mucous membrane and atrophic. In chronic colitis without atrophy of the mucous membrane, the latter is edematous, dull, granular, gray-red or red, with multiple hemorrhages and erosions. The prismatic epithelium undergoes desquamation and thickening. The number of goblet cells in the crypts increases, and the crypts are shortened, with an enlarged lumen. The mucous membrane is infiltrated with lymphocytes, plasma cells, eosinophils, with the presence of hemorrhages. The degree of infiltration can be moderate to severe diffuse. In chronic atrophic colitis, the prismatic epithelium thickens, the number of crypts decreases, and smooth muscle elements are hyperplastic. In the mucous membrane, histiolimphocytic infiltration and proliferation of connective tissue predominate. Nonspecific ulcerative colitis is a chronic relapsing disease that is manifested by inflammation of the colon with suppuration, ulceration, hemorrhages and outcome in sclerotic deformation of the wall. This is an allergic disease characterized by autoimmune aggression. Localized in the rectum, sigmoid or transverse colon. Sometimes the pathological process is localized throughout the colon. Morphologically, acute and chronic forms of nonspecific ulcerative colitis are distinguished. In the acute form, the intestinal wall is edematous, hyperemic, with multiple erosions and irregularly shaped superficial ulcers. Sometimes ulcers can penetrate deep into the muscle layer. At the bottom of the ulcer and in the zone of necrosis, vessels with fibrinoid necrosis and erosion of the walls are visible. Sometimes the ulcer perforates and intestinal bleeding occurs. Individual ulcers granulate and form granulomatous pseudopolyps. The mucous membrane is infiltrated with lymphocytes, plasma cells and eosinophils. In the chronic form, a sharp deformation of the intestine is noted - it becomes shorter, thickens and thickens. The intestinal lumen narrows. Reparative-sclerotic processes prevail. Ulcers granulate and scar, epithelialize incompletely. Pseudopolyps are formed. In the vessels there is a productive endovasculitis, the walls are sclerosed. Inflammation is productive and manifests itself in the form of infiltration of the intestinal wall with lymphocytes, histiocytes, and plasma cells. Crohn's disease Crohn's disease is a chronic relapsing disease of the gastrointestinal tract characterized by nonspecific granulomatosis and necrosis. The cause of this disease is unknown. Autoimmune processes take place in the intestines. The small intestine is most commonly affected. Pathological anatomy. The mucous membrane is thickened, edematous, tuberous (reminiscent of a cobblestone pavement) due to the alternation of long, narrow and deep ulcers, which are arranged in parallel rows along the length of the intestine. There may also be slit-like ulcers located across the intestine. The serous membrane is covered with adhesions and multiple whitish nodules. The intestinal lumen is narrowed, and fistulous passages are formed in the thickness of the intestine. Microscopically manifested by nonspecific granulomatosis, which covers all layers of the intestinal wall. Granulomas have a sarcoid-like structure and consist of epithelioid and giant cells of the Pirogov-Langhans type. The submucosal layer is edematous and diffusely infiltrated by lymphocytes, histiocytes, and plasma cells. Crohn's disease is considered a precancerous condition of the intestine. Appendicitis Appendicitis is an inflammation of the appendix. There are two clinical and anatomical forms of appendicitis - chronic and acute appendicitis. Acute appendicitis can be morphologically presented as simple, superficial and destructive. Acute appendicitis is a disorder of blood and lymph circulation in the form of stasis in capillaries and venules, edema, hemorrhages, accumulation of siderophages, as well as marginal standing of leukocytes and leukodiapedesis. With the superficial form of appendicitis, against the background of dyscirculatory changes, foci of exudative purulent inflammation of the mucous membrane appear. At the top of the focus, superficial defects of the epithelium are noted. Further processes are irreversible and represent destructive appendicitis. The leukocytic infiltrate extends to the entire thickness of the appendix wall, and phlegmonous appendicitis develops. The serous membrane is dull and full-blooded with a fibrinous coating. If multiple pustules appear, then they speak of apostematous appendicitis, and if ulcerations appear, they speak of phlegmonous-ulcerative appendicitis. The gangrenous process completes all of the above. Chronic appendicitis is characterized by sclerotic and atrophic processes, against which inflammatory-destructive changes may appear. Granulation tissue grows in the wall and lumen of the intestine, then matures and turns into scar tissue. Thus, all the walls of the process are sclerosed and atrophied, while the lumen of the appendix narrows. Adhesions appear between the appendix and surrounding tissues. Intestinal tumors Benign tumors are represented by an adenoma and are localized in the rectum, then in frequency - in the sigmoid, transverse, blind and thin. Among intestinal adenomas, tubular, tubular-villous and villous are distinguished. A villous adenoma is a pink-red tissue with a villous surface. Cancer is more common in the large intestine than in the small intestine. In the small intestine, the pathological process is more often localized in the region of the Vater nipple. Depending on the nature of growth, exophytic (plaque-like, polypous and large-tuberous) and endophytic (ulcerative and diffuse-infiltrative) are distinguished. Among the histological types of bowel cancer are adenocarcinoma, mycinous adenocarcinoma, cricoid, squamous, glandular squamous, undifferentiated and unclassified cancer. LECTURE No. 15. Diseases of the liver, gallbladder and pancreas 1. Liver disease Hepatosis Hepatosis is a liver disease characterized by dystrophy and necrosis of hepatocytes. May be hereditary or acquired. Toxic liver dystrophy develops as a result of a viral infection, allergies and intoxication. Microscopically, in the first days, fatty degeneration of hepatocytes of the centers of the lobules is noted, quickly replaced by their necrosis and autolytic decay with the formation of fat-protein detritus, in which there are crystals of leucine and tyrosine. Progressing, the pathological process captures all parts of the lobules by the 2nd week. This stage is called the stage of yellow dystrophy. On the 3rd week, red dystrophy begins to develop, which is manifested by a decrease in the size of the liver and a red color. At the same time, fat-protein detritus is phagocytosed and resorbed, the stroma is exposed, and sinusoids overflowing with blood are visualized. The result is postnecrotic cirrhosis of the liver. Fatty liver is a chronic disease characterized by increased accumulation of fat in hepatocytes. The reason is metabolic and endocrine disorders. In this case, the liver is large, yellow or red-brown, its surface is smooth. Fat is determined in hepatocytes. Lipids push the preserved organelles to the periphery. With severe hepatosis, liver cells die, and fatty cysts form. In terms of prevalence, disseminated obesity (single hepatocytes are affected), zonal (groups of hepatocytes) and diffuse obesity are distinguished. Obesity of hepatocytes can be dusty, small- and large-drop. There are three stages of fatty hepatosis - simple obesity, obesity in combination with necrobiosis of hepatocytes and mesenchymal cell reaction, and obesity with the beginning restructuring of the lobular structure of the liver. Hepatitis Hepatitis is an inflammation of the liver. According to the etiology, primary and secondary hepatitis are distinguished. Downstream - acute and chronic hepatitis. Primary hepatitis develops as a result of a hepatotropic virus, alcohol or drugs. Secondary hepatitis is the result of another disease, such as infection (yellow fever, typhoid fever, dysentery, malaria, sepsis, tuberculosis), intoxication (thyrotoxicosis, hepatotoxic poisons), lesions of the gastrointestinal tract, systemic connective tissue diseases, etc. Viral hepatitis occurs as a result of damage to the liver by a virus. There are viruses: A (HAV), B (HBV), C (HCV), D (HDV), E (HEV). The most common viruses are B and C. The following clinical and morphological forms of viral hepatitis are distinguished: acute cyclic (icteric), anicteric, necrotic (fulminant, malignant), cholestatic and chronic. In acute cyclic form, the stage of the peak of the disease and the stage of recovery are distinguished. In the stage of height, the beam structure of the liver is disturbed, and a pronounced polymorphism of hepatocytes is observed. Hydropic and balloon dystrophy of hepatocytes predominates, in various parts of the lobules there are focal and confluent necrosis of hepatocytes, Kaunsilmen's bodies. The portal and intralobular stromas are diffusely infiltrated by lymphocytes and macrophages with an admixture of plasma cells, eosinophilic and neutrophilic leukocytes. The number of reticuloendotheliocytes is increased. The cells of the infiltrate exit the portal stroma into the parenchyma of the lobule and destroy the hepatocytes of the border plate. Hepatocyte membranes are destroyed. In the recovery stage, the liver takes on normal dimensions, hyperemia decreases, the liver capsule is somewhat thickened, dull, and there are small adhesions between the capsule and the peritoneum. The degree of necrotic and dystrophic processes decreases microscopically, regeneration of hepatocytes is expressed. Lymphomacrophage infiltrate becomes focal. In less affected areas, restoration of the beam structure of the lobules is noted. Collagen fibers grow at the site of confluent necrosis of hepatocytes. With the anicteric form of hepatitis, the liver undergoes less pronounced changes. Microscopically, balloon dystrophy of hepatocytes with foci of necrosis is noted, Kaunsilmen's bodies are rare, and proliferation of stellate reticuloendothelial cells is pronounced. Lymphomacrophage and neutrophilic infiltrates do not destroy the border plate. Cholestasis is absent. Necrotic hepatitis is characterized by progressive necrosis of the liver parenchyma. The liver is reduced in size, becomes wrinkled and turns gray-brown or yellow. Microscopically, bridge-like necrosis of the liver is noted, among which are the accumulation of Kaunsilman's bodies, stellate reticuloendotheliocytes, lymphocytes, macrophages and neutrophils. The stasis of bile in the capillaries is pronounced. Hepatocytes are hydropically or balloon-dystrophic, with preserved parenchyma on the periphery of the lobules. In place of necrotic masses, a reticular stroma is formed, the lumen of the sinusoids is enlarged and plethoric with the presence of hemorrhages. The cholestatic form of hepatitis is based on intrahepatic cholestasis and inflammation of the bile ducts. Microscopically, signs of cholestasis predominate. The bile capillaries and ducts are filled with bile, the bile pigment accumulates in hepatocytes and in stellate reticuloendotheliocytes. Hepatocytes of the central sections of the lobules are in a state of hydropic or ballooning dystrophy, there are Kaunsilmen's bodies. The portal tracts are dilated and infiltrated with lymphocytes, macrophages, and neutrophils. The chronic form of hepatitis is represented by active and persistent hepatitis. In chronic active hepatitis, dystrophy and necrosis of hepatocytes develop. Characterized by cellular infiltration of the portal, periportal and intraportal sclerotic stroma of the liver. The degree of spread of necrosis is a criterion for setting the activity of the disease. Destruction of hepatocytes is combined with focal or diffuse proliferation of stellate reticuloendotheliocytes and cholangiol cells. Chronic persistent cholangitis is characterized by infiltration of lymphocytes, histiocytes, and plasma cells into sclerotic portal fields. Star-shaped reticuloendotheliocytes are hyperplastic, there are foci of necrosis of the reticular stroma. The structure of the hepatic lobules and the border plate is preserved. Dystrophic processes are minimally expressed. Hepatocyte necrosis is rare. Death in viral hepatitis occurs due to acute or chronic liver failure. Alcoholic hepatitis occurs due to alcohol intoxication. In the acute form of alcoholic hepatitis, the liver is dense and pale, with reddish areas. Hepatocytes are necrotic, infiltrated with neutrophils, and a large amount of alcoholic hyaline (Mallory bodies) appears in them. Cirrhosis of the liver Cirrhosis of the liver is a chronic disease characterized by structural changes in the liver and scarring. All pathological processes occurring in the liver and having a chronic nature are the causes of the development of cirrhosis of the liver. The main pathological processes in cirrhosis are dystrophy and necrosis of hepatocytes, perverted regeneration, diffuse sclerosis, as well as structural restructuring and deformation of the organ. The liver becomes dense, tuberous, as a rule, reduced in size, rarely enlarged. Macroscopically, there are types of cirrhosis: incomplete septal, small-nodular, large-nodular and mixed. With incomplete septal cirrhosis, there are no regenerator nodes, thin septa cross the liver parenchyma. With small-nodular - regenerator nodes of the same size (no more than 1 cm) and have a monolobular structure, the septa in them are narrow. With large-nodular cirrhosis, the nodes are large (up to 5 cm). With mixed cirrhosis, the nodes are of various sizes. Regenerator nodes, or false lobules, have an irregular structure of the vessels and an incorrect course of the beams. Microscopically, monolobular (captures one hepatic lobule), multilobular (captures several hepatic lobules) and monomultilobular cirrhosis are isolated. Hydropic or balloon dystrophy and necrosis occur in hepatocytes. Regeneration intensifies and regenerator nodes appear, surrounded on all sides by connective tissue. Diffuse fibrosis develops and anastomoses form. All of the above pathological processes are irreversible, which leads to the constant progression of liver failure and, consequently, to the death of the patient. Liver cancer is very rare. As a rule, it is formed against the background of cirrhosis of the liver. Microscopically, there are nodular (the tumor is represented by one or more nodes), massive (the tumor occupies a massive part of the liver) and diffuse cancer. Special forms include small and peduncular cancer. The liver is sharply enlarged, with nodular cancer it is bumpy and moderately dense. By the nature of growth, expansive, infiltrating and mixed are distinguished; substitutive growth is also possible along sinusoids. Histiogenetically distinguish between hepatocellular (hepatocellular), cancer of the epithelium of the bile ducts (cholangiocellular), mixed (hepatocholangiocellular) and hepatoblastoma. Histologically, cancer can be tubular, trabecular, acinar, solid, and clear cell. The degree of differentiation may be different. The death of the patient occurs from bleeding and cachexia. 2. Diseases of the gallbladder Cholecystitis The most common disease is cholecystitis, which can be acute or chronic. In acute cholecystitis, catarrhal, fibrinous or purulent inflammation develops. It can be complicated by perforation of the bladder wall and biliary peritonitis. If the bladder is intact, then bladder empyema, purulent cholangitis, cholangiolitis, pericholecystitis are formed with the formation of adhesions. Chronic cholecystitis is a consequence of acute cholecystitis and is manifested by atrophy of the mucous membrane, histiolimphocytic infiltration, sclerosis and petrification of the bladder. Gallbladder stones stop the lumen of the bile ducts at the level of the liver and below, causing hepatic and subhepatic jaundice. gallbladder cancer Gallbladder cancer develops against the background of calculous cholecystitis and is localized in the neck or bottom of the bladder. Cancer usually has the structure of adenocarcinoma. 3. Diseases of the pancreas Diseases of the pancreas are represented by inflammatory and oncological processes. pancreatitis Pancreatitis is an inflammation of the pancreas. Acute and chronic pancreatitis are distinguished along the course. In acute pancreatitis, the pancreas is edematous with white-yellow areas of necrosis (fat necrosis), hemorrhages, suppuration foci, false cysts and sequesters. With the predominance of one or another change, they speak of hemorrhagic or purulent pancreatitis. Chronic pancreatitis is characterized by the predominance of sclerotic and atrophic processes in combination with the regeneration of acinar cells and the formation of regenerative adenomas. Sclerotic changes lead to impaired patency of the duct and the formation of cysts. Cicatricial deformity of the gland is combined with tissue calcification. The gland decreases in size and becomes dense, like cartilage. Pancreas cancer Pancreatic cancer can develop in any department, but more often - in the head of the pancreas. Cancer develops from the epithelium of the ducts (adenocarcinoma) or from the acini of the parenchyma (acinar or alveolar cancer). The tumor has the appearance of a gray-white node. The death of the patient comes from metastases. LECTURE No. 16. Diseases of the kidneys In renal pathology, two main groups of diseases are distinguished: glomerulopathies and tubulopathies. The basis of glomerulopathies is a violation of the glomerular apparatus of the kidneys, and the basis of tubulopathies is predominantly damage to the tubules. In the first case, glomerular filtration is disturbed, and in the second, the concentration, reabsorption and secretory functions of the tubules. A separate and large group of diseases are interstitial nephritis, pyelonephritis, nephrosclerosis and nephrolithiasis, the basis of which is chronic renal failure. 1. Glomerulopathies glomerulonephritis Glomerulonephritis is an infectious-allergic or unidentified disease, which is based on bilateral diffuse or focal non-purulent inflammation of the glomerular apparatus of the kidneys with the presence of renal and extrarenal manifestations. Renal symptoms include oliguria, proteinuria, hematuria, cylindruria, and extrarenal symptoms include arterial hypertension, left ventricular and atrial hypertrophy, dysproteinemia, edema, hyperazotemia, and uremia. Classification 1. By etiology, glomerulonephritis of established etiology (viruses, bacteria, protozoa) and unknown etiology are distinguished. 2. According to nosology, primary glomerulonephritis is distinguished as an independent disease, and secondary glomerulonephritis (as a manifestation of another disease). 3. According to the pathogenesis, glomerulonephritis can be immunologically conditioned and immunologically unconditioned. 4. Downstream - acute, subacute and chronic. 5. Topographically distinguish intracapillary (pathological process is localized in the vascular glomerulus) and extracapillary (pathological process in the glomerular capsule) glomerulonephritis. 6. By the nature of inflammation - exudative, proliferative and mixed. 7. By prevalence - diffuse and focal glomerulonephritis. In acute glomerulonephritis, the kidneys are enlarged, swollen, the pyramids are dark red, the bark is grayish-brown in color with small red specks on the surface and incision, or with grayish translucent dots (variegated kidney). In the first days of the disease, the glomeruli are hyperemic. Then they are infiltrated by neutrophils, proliferation of endothelial and mesangial cells appears. All these processes are reversible, but in severe cases, when fibrinoid necrosis of capillaries appears, the process becomes irreversible. In subacute glomerulonephritis, as a result of the proliferation of the epithelium of the capsule, podocytes and macrophages, crescent formations ("crescents") appear, which compress the glomerulus. Capillary loops undergo necrosis, and fibrin clots form in their lumen. Fibrin is also located in the cavity of the capsule, where it contributes to the transformation of crescents into fibrous adhesions or hyaline fields. Nephrocytes undergo dystrophy, the stroma is edematous and infiltrated. Macroscopically: the kidneys are enlarged, flabby, the cortical layer is wide, swollen, yellow-gray, dull with red specks and well demarcated from the dark red medulla of the kidney. In the chronic course of glomerulonephritis, the kidneys are wrinkled, reduced in size, dense with a fine-grained surface. On the section, the layer of renal tissue is thin, the tissue is dry, anemic, gray in color. Microscopically, the tubules and glomeruli are atrophied and replaced by connective tissue, the capsule is thickened, and the capillary loops are sclerotic. The lumen of the tubules is expanded, and the epithelium is thickened. Arterioles sclerosed and hyalized. Mesangial and fibroplastic types are distinguished: mesangial glomerulonephritis develops as a result of proliferation of mesangiocytes in response to deposits under the epithelium and in the mesangium of immune complexes. The mesanglion of the vessels of the glomeruli of the kidneys expands, the processes of mesangiocytes are forced out to the periphery of the capillary loops, the endothelium exfoliates from the membrane, the tubules degenerate and atrophy, and the stroma undergoes cellular infiltration and sclerosis. Macroscopically, the kidneys are dense, pale, with yellow spots in the cortical layer. Fibroplastic glomerulonephritis is characterized by sclerosis and hyalinosis of capillary loops and the formation of adhesions in the capsule cavity. The kidneys are dense, gray-red and reduced in size, with the presence of small depressions. The outcome of chronic glomerulonephritis is unfavorable. The pathological process leads to renal failure, which is manifested by azotemia uremia. The nephrotic syndrome is characterized by proteinuria, dysproteinemia, hypoproteinemia, hyperlipidemia, and edema. There are primary (idiopathic) nephrotic syndrome and secondary - as a manifestation of renal disease. Primary nephrotic syndrome can be manifested by three diseases: 1) lipoid nephrosis; 2) membranous nephropathy; 3) focal segmental sclerosis. Lipoid nephrosis is manifested by minimal changes in the glomerular apparatus and is characterized by the loss of their small islets by podocytes. As a result of the fusion of podocytes with the membrane, it thickens and there is a slight expansion of the mesanglion. The tubules of the main sections are dilated, the epithelium is swollen, contains hyaline drops, vacuoles, neutral fats and cholesterol. Dystrophy, necrobiosis, atrophy and desquamation of the tubular epithelium are combined with its regeneration. In the lumen of the tubules there are many hyaline, granular and waxy cylinders. The stroma is edematous, the lymphatic vessels are dilated. There are many lipids, lipophages and lymphoid elements in the interstitium. Macroscopically, the kidneys are enlarged, flabby, the capsule is removed easily, exposing a yellowish smooth surface. The cortical layer on the cut is wide, yellow-white or pale gray, the pyramids are gray-red (large white buds). Membranous nephropathy develops as a result of damage by immune complexes. At the same time, the kidneys are enlarged, pale pink or yellow, with a smooth surface. Microscopically, there is a diffuse thickening of the walls of the glomerular capillaries with a slight proliferation of mesangiocytes. The thickening occurs due to the neoformation of the substance of the basement membrane, due to the deposits of circulating complexes, which are located in the form of outgrowths in the direction of the podocytes. All of the above is called membranous transformation, which ends with sclerosis and hyalinosis of the glomerular capillaries. Focal segmental glomerular sclerosis (hyalinosis) can be primary or secondary (associated with lipoid nephrosis). Sclerosis and hyalinosis develop in the juxtamedullary glomeruli. Lipids are always present in hyaline masses and mesangiocytes - in the form of foam cells. Renal amyloidosis Amyloidosis of the kidneys, as a rule, is a secondary disease (with rheumatoid arthritis, tuberculosis, bronchiectasis, etc.), and in congenital pathology it is of a primary nature. In the course of amyloidosis, there are latent, proteinuric, nephrotic and azotemichesky stages. In the latent stage, the kidneys are not macroscopically changed. The glomerular membrane is thickened and double-circuited, the lumens of the aneurysm are dilated. The cytoplasm of the epithelium of the tubules is impregnated with protein granules. In the intermedial zone and pyramids, the stroma is impregnated with plasma proteins. In the proteinuric stage, amyloid appears not only in the pyramids, but also in the glomeruli. It is deposited in the mesangium and capillary loops, as well as in arterioles. The epithelium of the tubules is subject to hyaline-droplet or hydropic dystrophy, and cylinders are found in their lumen. Macroscopically, the kidneys are changed - enlarged and dense, the surface is pale gray or yellow-gray. On the section, the cortical layer is wide, matte, and the medulla is gray-pink, sebaceous (large sebaceous kidney). In the nephrotic stage, the amount of amyloid increases, localized in capillary loops, arterioles and arteries, along the tubular membrane. In the pyramids and the intermedial zone sclerosis; amyloidosis increases and is diffuse. The tubules are dilated and clogged with cylinders. Macroscopically, there is an even greater increase in the kidneys - they are more dense and waxy (large white amyloid kidney). In the azotemic stage, an increase in the growth of amyloid and sclerotic processes is noted, which increases the number of dying nephrons. Macroscopically, there is a decrease in the kidneys to normal sizes due to sclerosis. They become very dense and have an uneven surface (due to sclerotic retractions). At this stage, extrarenal manifestations of the disease are well expressed. The outcome of amyloidosis is chronic renal failure. 2. Tubulopathies Acute renal failure Acute renal failure is a syndrome that occurs due to necrosis of the epithelium of the tubules and deep disorders of blood and lymph circulation. In the development of this pathology, two main reasons are distinguished - intoxication and infection. Pathologically, there are 3 stages. 1. The initial shock stage is characterized by venous plethora of the intermedial zone and pyramids with focal ischemia of the cortical layer (collapsed capillaries). The epithelium of the tubules of the main departments is subject to hyaline droplet, hydropic or fatty degeneration. The lumens of the tubules are unevenly dilated, contain cylinders, and sometimes myoglobin crystals. 2. The oligoanuric stage is characterized by pronounced necrotic processes in the tubules of the main departments. The basement membrane of the distal tubules undergoes destruction (tubulorhexis). Edema of the interstitium increases, and leukocyte infiltration and hemorrhage join it. The cylinders overlap the nephron. 3. The stage of recovery of diuresis is characterized by a decrease in edema of infiltration of the kidney, and many glomeruli become full-blooded. Foci of sclerosis are formed. The macroscopic picture of the kidneys in all stages is the same. The kidneys are enlarged, swollen, edematous, the fibrous capsule is tense and easily removed. The cortical layer is wide, pale gray in color and sharply demarcated from the dark red pyramids; hemorrhages are noted in the pelvis. The outcome is different: both recovery and death are possible. 3. Interstitial nephritis There are the following types of interstitial nephritis. 1. Tubulo-interstitial nephritis is a pathological process characterized by immuno-inflammatory lesions of the interstitium and renal tubules. The reasons are varied - intoxication, infection, metabolic disorders, immunological and sensitizing processes, oncology and hereditary pathology. There are primary and secondary tubulo-interstitial nephritis (with Goodpasture's syndrome, kidney rejection reactions). In acute tubulo-interstitial nephritis, edema and infiltration of the interstitium of the kidneys occur. Depending on the cells that infiltrate, lymphohistiocytic (lymphocytes and macrophages), plasmacytic (plasmocytes and plasmablasts), eosinophilic (eosinophils) and granulomatous (granulomas) variants are isolated. The cellular infiltrate spreads perivascularly, destroying nephrocytes. In chronic tubulo-interstitial nephritis, lymphohistiocytic infiltration of the stroma is combined with sclerosis, and degeneration of nephrocytes - with their regeneration. Among the cells of the infiltrate, lymphocytes and macrophages predominate, and the basement membrane is thickened. The outcome is nephrosclerosis. 2. Pyelonephritis is an infectious disease characterized by damage to the renal pelvis, calyces and kidney substance, with a predominant lesion of the interstitial tissue. Pyelonephritis can be acute and chronic. In acute pyelonephritis macroscopically the kidney is enlarged, the tissue is swollen, full-blooded, the capsule is easily removed. The cavities of the pelvis and calyces are enlarged, filled with cloudy urine or pus, their mucous membrane is dull, with foci of hemorrhage. On the section, the renal tissue is variegated, with the presence of yellow-gray areas surrounded by a zone of plethora and hemorrhage. Microscopically revealed plethora and leukocyte infiltration of the pelvis and calyx, foci of necrosis of the mucous membrane. The interstitial tissue is edematous and infiltrated with leukocytes. The tubules are prone to dystrophy, and their lumens are clogged with cylinders. The process is either focal or diffuse. In chronic pyelonephritis, the processes of sclerosis are combined with exudative-necrotic ones: the calyces and pelvis are sclerosed, the mucous membrane is polyposis, the transitional epithelium is replaced by a multilayer one. Chronic interstitial inflammation with proliferation of connective tissue is expressed in the kidney tissue. The tubules are dystrophic and atrophied, and the remaining ones are sharply stretched, their epithelium is flattened, the lumen is filled with colloid-like contents. Arteries and veins are sclerotic. With a long course, a pyelonephritic wrinkled kidney develops. 4. Kidney stone disease Kidney stone disease (nephrolithiasis) is a disease characterized by the formation of stones in the renal calyces, pelvis and ureters. The process is chronic. As a result of violation of the outflow of urine, pyelectasis and hydronephrosis occur with atrophy of the renal parenchyma. The pelvis and ureter are dilated, inflammation joins, which leads to pyelonephritis up to the melting of the parenchyma. After the inflammatory process, the parenchyma is sclerosed or completely replaced by sclerosed adipose tissue (fat replacement of the kidney). At the site of obturation with a stone, a bedsore with perforation of the ureter can form. 5. Polycystic kidney disease Polycystic kidney disease is an inherited kidney disease with bilateral cystic parenchyma. As a rule, this is a long-term disease that is asymptomatic. Early manifestations of this disease indicate a malignant course. Pathological anatomy The kidneys in this disease resemble bunches of grapes, the tissue of which consists of many cysts of various sizes and shapes, filled with serous fluid, colloidal masses or semi-liquid chocolate-colored contents. The cysts are lined with cuboidal epithelium. Sometimes a wrinkled vascular glomerulus is located in the wall of the cyst. The renal tissue between the cysts is atrophied. The outcome is unfavorable - patients die of renal failure. 6. Nephrosclerosis Nephrosclerosis is a flattening and deformation of the kidneys due to the growth of connective tissue. Macroscopically, the kidneys are dense, the surface is large- and small-hilly. Kidney tissue undergoes structural restructuring due to the growth of connective tissue. The kidney shrinks. A manifestation of nephrosclerosis is chronic renal failure. A striking clinical sign of chronic renal failure is uremia. In this case, autointoxication occurs, all organs are affected by urea, primarily organs and systems that perform the excretory function of the body (skin, lungs, gastrointestinal tract). The reaction with xanth hydrochloride makes it possible to detect urea in all organs. As a result of the accumulation of urochrome, the skin becomes gray-earthy, and hypersecretion of sweat glands, rashes and hemorrhages are noted. Uremic pulmonary edema, laryngitis, tracheitis are characteristic, pharyngitis, gastritis, enterocolitis are common, fatty degeneration occurs in the liver. Serous, serofibrinous or fibrinous pericarditis, uremic myocarditis are very often found. The brain is pale and edematous, sometimes foci of softening with hemorrhages develop. The spleen is enlarged. With prolonged hemodialysis, chronic suburemia develops. At the same time, metabolic damage (myocardial necrosis), productive inflammation (adhesive pericarditis, obliteration of the cavity of the heart shirt), changes in bones (osteoporosis, osteosclerosis, amyloidosis) and the endocrine system (parathyroid hyperplasia) dominate. 7. Tumors of the kidneys Kidney tumors are classified as follows. 1. Epithelial tumors: 1) adenoma (dark cell, clear cell and acidophilic); 2) renal cell carcinoma (clear cell, granular cell, glandular, sarcomatoid, mixed cell); 3) nephroblastoma or Wilms tumor. 2. Mesenchymal tumors are formed from connective and muscle tissue, from blood and lymphatic vessels, they are benign and malignant. 3. Tumors of the renal pelvis: 1) benign (transitional papilloma); 2) cancer of the pelvis (transitional cell, squamous and glandular). LECTURE No. 17. Diseases of the genital organs and the mammary gland Diseases of the genital organs and the mammary gland are divided into dyshormonal, inflammatory and tumor. 1. Dishormonal diseases These include nodular hyperplasia and prostate adenoma, glandular hyperplasia of the uterine mucosa, endocervicosis, adenomatosis and cervical polyps, benign breast dysplasia. 1. Nodular hyperplasia and prostate adenoma are divided into 3 forms according to the histological type: 1) glandular hyperplasia is characterized by an increase in glandular elements; 2) muscular-fibrous (stromal) hyperplasia is characterized by the appearance of a significant number of smooth muscle fibers, among which atrophied glandular elements are located, the lobulation of the gland is disturbed; 3) mixed form is a combination of the above forms. 2. Glandular hyperplasia of the uterine mucosa develops as a result of hormonal imbalance and the ingestion of an excess amount of folliculin or progesterone. The mucous membrane of the uterus is thickened with the presence of polyposis outgrowths. The glands are tortuous, have an elongated shape. When cysts appear, they speak of glandular cystic hyperplasia. Against the background of these processes, an inflammatory process can join with a transition to sclerosis - up to uterine cancer. 3. Endocervicosis is an accumulation of glands in the thickness of the vaginal part of the cervix with altered epithelium; distinguish: 1) proliferating endocervicosis, which is characterized by the neoplasm of glandular structures developing from the cambial elements of the prismatic epithelium of the cervical canal; 2) simple endocervicosis with no signs of neoplasm; 3) healing endocervicosis, manifested by ingrowth into the glands of the squamous epithelium and replacing it with a prismatic one. 4. Adenomatosis of the cervix is a collection of glandular formations under the integumentary epithelium of the vaginal part of the uterus, lined with one layer of cuboidal epithelium. With polyps, the pathological process is localized in the canal, less often in the vaginal part. Polyps are formed by prismatic mucus-forming epithelium. 5. Benign dysplasia of the mammary gland is characterized by impaired differentiation of the epithelium and its atypia and impaired histostructures; differ: 1) non-proliferative form, when the connective tissue grows with areas of hyalinosis, in which atrophic lobules and cystic dilated ducts are located; ducts and cysts are lined with atrophic or high epithelium; microscopically - a dense whitish knot; 2) the roliferative form is characterized by proliferation and growth of the epithelium and connective tissue. Against the background of the above pathological processes, cancer can develop, so they are considered precancerous conditions. 2. Inflammatory diseases of the genital organs and mammary gland Inflammatory diseases of the genital organs and mammary gland are classified as follows. 1. Endometritis - inflammation of the uterine mucosa. In the acute form, the mucous membrane is covered with a purulent or putrefactive coating of a gray-red color. With the transition of the inflammatory process to the vessels of the myometrium, purulent metritis and thrombophlebitis develop. In the chronic form of endometritis, the mucous membrane is plethoric, infiltrated with a variety of cells (neutrophils, lymphoid cells, plasma cells). The epithelium of the glands is in a state of increased proliferation. With a long course, the glands atrophy, the stroma of the mucous membrane is fibrosed, and atrophic endometritis is formed. If the mucous membrane is hyperplastic, then they speak of hypertrophic endometritis. 2. Mastitis - inflammation of the mammary gland. Acute mastitis occurs in the postpartum period and is phlegmonous in nature, and chronic is its consequence and is purulent in nature. 3. Orchitis - inflammation of the testicle. May be acute and chronic. In the acute form of orchitis, purulent inflammation develops. Chronic orchitis is characterized by diffuse or granulomatous inflammation. 4. Prostatitis - inflammation of the prostate gland; distinguish between acute and chronic. There are 3 forms of acute prostatitis: 1) the catarrhal form is characterized by the occurrence of purulent catarrh of the ducts of the prostatic glands, the vessels are plethoric, and the interstitium of the gland is edematous; 2) the follicular form is manifested by changes in the ducts and the addition of foci of inflammatory infiltration of the glands; 3) the parenchymal form is manifested by diffuse leukocyte infiltration, abscesses and foci of granulations. In chronic prostatitis, lymphohistiocytic infiltration of the gland stroma, proliferation of granulation and scar tissue predominate. Atrophy of the glands is combined with proliferation and metaplasia of the epithelium of the ducts, resulting in the formation of cribriform and papillary structures. 3. Tumors of the genital organs and mammary glands Tumors are as follows. 1. Uterine cancer is topographically divided into cancer of the cervix and body of the uterus. Cervical cancer can be non-invasive and invasive. Distinguish between cancer in the vaginal part of the cervix (grows exophytically and ulcerates early) and cancer of the cervical canal (has endophytic growth). Histologically, squamous, glandular and glandular squamous cell carcinoma of the cervix is isolated; also isolated endometrioid adenocarcinoma of the cervix. Cancer of the uterine body is more often an exophytic growth in the form of a cauliflower or a polyp on a wide base. The tumor is prone to decay and ulceration. Histologically, it looks like an adenocarcinoma. 2. Testicular cancer is the result of malignancy of epithelial serous or mucinous tumors and looks like a tuberous node of various sizes. Testicular cancer is morphologically represented by seminoma, teratoblastoma and embryonic cancer. 3. Breast cancer is microscopically represented by nodular and diffuse forms, as well as cancer of the nipple and nipple field (Paget's cancer). Nodular cancer is characterized by a node of various diameters, which can be dense and permeated with whitish layers, or can be soft and juicy on the cut and easily disintegrate. Diffuse cancer covers almost the entire gland, up to the skin, forming a cancerous ulcer. According to the histological structure, they differ: 1) non-infiltrative breast cancer (intralobular and intraductal); 2) infiltrating cancer (ductal, lobular, Paget's disease). 4. Prostate cancer. The gland is enlarged, dense, bumpy, on the cut consists of intertwining strands of fibrous tissue, between which there is a gray-yellow cancerous tissue. Microscopically, cancer has the structure of adenocarcinoma, less often undifferentiated cancer. LECTURE No. 18. Diseases of the endocrine glands The human endocrine system consists of two systems - the peripheral endocrine system and the hypothalamic-pituitary system. They are closely related and able to regulate each other. Diseases of the endocrine system can be congenital or acquired. They manifest as hypofunction, hyperfunction and dysfunction. Structural reorganization manifests itself in the form of dystrophy, atrophy or dysplasia. 1. Pituitary disorders Pituitary disorders are as follows. 1. Acromegaly occurs as a result of an excess of growth hormone. It is manifested by stimulation of the growth of connective, cartilaginous and bone tissue, as well as the parenchyma and stroma of internal organs (heart, kidneys, liver). The cause is adenocarcinoma of the anterior pituitary gland. 2. Pituitary dwarfism develops with congenital underdevelopment of the pituitary gland or in violation of its tissue in childhood. It is manifested by general underdevelopment with preserved proportionality. The reproductive organs are underdeveloped. 3. Cerebro-pituitary cachexia manifests itself in increasing cachexia, atrophy of internal organs and a decrease in the function of the genital organs. Microscopically, in the anterior lobe of the pituitary gland, foci of necrosis or scars are localized in their place. In the diencephalon, dystrophic or inflammatory changes are noted. Sometimes brain changes predominate over pituitary ones. 4. Itsenko-Cushing's disease occurs due to hypersecretion of adrenocorticotropic hormone. There is a bilateral hyperplasia of the adrenal cortex with excessive production of glucocorticosteroids. Clinically manifested by obesity (mainly male type). There is a redistribution of subcutaneous fat on the face (moon face) and trunk with thin limbs. Arterial hypertension, diabetes mellitus, secondary ovarian dysfunction, osteoporosis are characteristic. Purple-bluish striae form on the skin of the thighs and abdomen. 5. Adiposogenital dystrophy is characterized by pathological changes in the pituitary and hypothalamus, which develop as a result of a tumor or neuroinfection. It is manifested by progressive obesity, underdevelopment and a decrease in the function of the genital organs. 6. Diabetes insipidus occurs when the posterior lobe of the pituitary gland and the diencephalon are damaged. The antidiuretic hormone is switched off and, as a result, the concentration furcation of the kidneys is disturbed. It is clinically manifested by thirst (polydipsia) and diabetes (polydipsia). 2. Adrenal disorders Addison's disease or bronze disease. The disease is characterized by damage mainly to the cortical substance of the adrenal glands, while the production of glucocorticosteroids and sex hormones decreases or completely stops. Causes: metastases, autoimmune lesions, amyloidosis, hemorrhages, tuberculosis, disorders of the hypothalamic-pituitary system. There are hyperpigmentation of the skin and mucous membranes, myocardial atrophy, a decrease in the lumen of the aorta and great vessels. Islet cells of the pancreas are hyperplastic, the gastric mucosa is atrophied. Lymphoid tissue and thymus gland are hyperplastic. 3. Thyroid Goiter Goiter (struma) is an enlargement of the thyroid gland. Morphologically, goiter is divided into: 1) diffuse; 2) nodal; 3) diffuse-nodular. Histologically different: 1) colloid goiter; 2) parenchymal goiter. Colloidal goiter is histologically represented by follicles of various sizes, which are filled with colloid. The epithelium can grow in the form of papillae. There is a circulatory disorder in the gland, foci of necrosis and calcification are formed, the connective tissue grows. On cut, the goiter is nodular and dense. Parenchymal goiter is characterized by proliferation of the epithelium of the follicles. The epithelium grows in the form of solid structures with the formation of small follicle-like formations without colloid or with a small amount of it. The process is diffuse in nature and looks like a homogeneous fleshy tissue of a gray-pink color. Clinically distinguish: 1) endemic goiter; 2) sporadic goiter; 3) diffuse toxic goiter. Endemic goiter develops as a result of a lack of iodine in the water. In this case, the thyroid gland increases significantly in size, and can be colloidal or parenchymal in structure. The function of the gland is reduced. Sporadic goiter is histologically and morphologically diverse. The gland increases in size, does not suffer functionally, and can compress organs. In rare cases, moderate papillary proliferation of the epithelium of the follicles and the accumulation of infiltrates in the stroma of the gland are possible. Diffuse toxic (thyrotoxic) goiter. The reason is the production of autoantibodies to thyrocyte receptors. Morphologically, the degeneration of the prismatic epithelium of the follicles into a cylindrical one is noted, the epithelium undergoes proliferation with the formation of papillae, the stroma is lymphocytally infiltrated, the colloid changes its properties and poorly perceives dyes. The myocardium is hypertrophied, its interstitial tissue is edematous and lymphoid infiltrated, further developing interstitial sclerosis. In the liver, serous edema occurs with a transition to fibrosis. Nerve cells are dystrophically changed. The adrenal cortex atrophies. Lymphoid tissue is hyperplastic. Thyroiditis Thyroiditis is a true autoimmune disease. Microscopically, diffuse infiltration of the gland tissue by lymphocytes and plasma cells with the formation of lymphoid follicles is noted. The parenchyma of the gland is replaced by connective tissue. 4. Pancreas Diabetes Diabetes mellitus is a disease caused by relative or absolute insufficiency of insulin. Classification: 1) spontaneous diabetes (insulin-dependent type 1 and insulin-independent type 2); 2) gestational diabetes; 3) secondary diabetes; 4) latent diabetes. Risk factors for etiology and pathogenesis include: 1) genetically determined disorders in the function and number of β-cells (decrease in insulin synthesis, impaired conversion of preinsulin to insulin, abnormal insulin synthesis); 2) environmental factors, violation of the integrity and functioning of β-cells (viruses, autoimmune diseases, obesity, increased activity of the adrenergic nervous system). Insulin deficiency disrupts glycogen synthesis, increases blood sugar (hyperglycemia), and sugar appears in the urine (glucosuria). Due to neoglycogenesis, glucose synthesis occurs, which leads to hyperlipidemia, acetonemia and ketonemia. All of these substances lead to acidosis. Vessels are affected and diabetic microangiopathy and macroangiopathy occur. Pathological anatomy. First of all, the islets of the pancreas are affected, changes occur in the liver, vascular bed and kidneys. The pancreas is reduced in size, its lipomatosis and sclerosis occur. Most islets undergo atrophy and hyalinosis, while other islets hypertrophy compensatory. The liver is enlarged and the liver cells become fatty. Diabetic macroangiopathy is manifested by atherosclerosis of elastic and muscular arteries. In diabetic microangiopathy, the basement membrane of the microvasculature undergoes plasmorrhagic impregnation, and later sclerosis and hyalinosis. This creates lipogyalin. This process is generalized. The kidneys in diabetes are affected in the form of diabetic glomerulonephritis and glomerulosclerosis. There is a proliferation of mesangial cells, in which the formation of a membrane-like substance is enhanced, which leads to hyalinosis of the mesanglion and death of the glomeruli. The process can be diffuse, nodular and mixed. An exudative manifestation of diabetic nephropathy is possible, while fibrin caps form on the capillary loops of the glomeruli, the epithelium of the nodal segment of the nephron changes, it becomes high with a light translucent membrane in which glycogen is detected. Death in diabetes occurs as a result of gangrene of the extremities, myocardial infarction, uremia, and rarely from diabetic coma. LECTURE No. 19. Diseases of the central nervous system Diseases of the central nervous system are divided into: 1) dystrophic (degenerative) diseases characterized by a predominance of damage to neurons of various localizations; 2) demyelinating diseases, characterized by a primary lesion of the myelin sheaths (primary demyelination) or axons (secondary demyelination); 3) inflammatory diseases are divided into meningitis, encephalitis and meningoencephalitis. 1. Alzheimer's disease Alzheimer's disease is clinically manifested by severe intellectual disorders and emotional lability, while focal neurological symptoms are absent. Morphologically characterized by atrophy of the brain, mainly - frontal, temporal and occipital regions. Hydrocephalus may develop. Microscopically, in the cortex of the atrophic lobes of the brain, the hypocampus and the amygdala, senile plaques, neurofibrillary plexuses (glomeruli), damage to neurons, and Hirano bodies are found. Prussic plaques and neurofibrillary plexuses are located in all parts of the cerebral cortex, with the exception of motor and sensory areas. Neurofibrillary plexuses are more often found in the nucleus basalis of Meinert, and Hirano bodies are found in the neurons of the hippocampus. Senile plaques consist of foci of amyloid deposition surrounded by pairwise twisted filaments; microglial cells and sometimes astrocytes are located along the periphery of the plaques. Neurofibrillary plexuses are represented by helical pairwise twisted filaments, which are detected by silver impregnation. They look like glomeruli or nodules of fibrillar material and straight tubules in the cytoplasm of neurons. Neurons in the affected areas decrease in size, their cytoplasm vacuolizes and contains agrophilic granules. Hirano bodies are represented by an accumulation of oriented actin fragments, localized in the proximal dendrites and have the form of eosinophilic inclusions. 2. Charcot's disease Amyotrophic lateral sclerosis (Charcot's disease) is a progressive disease of the central nervous system, which is characterized by simultaneous damage to the motor neurons of the anterior and lateral columns of the spinal cord and peripheral nerves. It is clinically manifested by the development of spastic paresis of the muscles of the hands with further attachment of muscle atrophy, increased tendon and periosteal reflexes. The reason is unknown. Pathological anatomy The anterior motor roots of the spinal cord are atrophic, they are thinned, gray in color, and the posterior sensory roots remain unchanged. The lateral corticospinal tracts are thickened, whitish in color and delimited from other tracts by a clear line. Possible atrophy of the precerebral gyrus of the brain. Skeletal muscles atrophy. At microscopy in the anterior horns of the spinal cord, pronounced changes in nerve cells are noted - they are wrinkled or look like threads, extensive fields of loss of neurons are found. In the nerve fibers of the spinal cord, demyelination, uneven swelling, followed by disintegration and death of the axial cylinders, are determined. Also, this process can spread to peripheral nerves. Reactive proliferation of glial cells is noted in the pyramidal tracts. The cause of death in such patients is cachexia or aspiration pneumonia. 3. Multiple sclerosis Multiple sclerosis (multiple sclerosis) is a chronic progressive disease characterized by the formation of scattered foci of demyelination in the brain and spinal cord, in which glia grows with the formation of foci of sclerosis (plaques). The cause of the disease is unknown, although a viral etiology is suspected. Externally, the superficial sections of the brain and spinal cord are little changed. Sometimes there may be swelling and thickening of the meninges. On sections of the brain and spinal cord, a large number of gray plaques scattered in the white matter with clear outlines and up to several centimeters in diameter are found. Plaques can merge with each other. The most common localization is around the ventricles of the brain, in the spinal and medulla oblongata, the brain stem and visual tubercles. The optic nerves, chiasm, and optic pathways are often affected. Microscopically, in the early stage, foci of demyelination around the blood vessels are found. Vessels are surrounded by lymphocytes and mononuclear cells, axons are relatively unchanged. Myelin sheaths swell, their contours are uneven with the presence of spherical thickenings along the fibers. Subsequently, fragmentation and disintegration of the myelin sheaths occur. The decay products are utilized by microglial cells, which turn into granular balls. In fresh lesions, changes in axons can be detected, which become inflated and have an uneven thickness. In the stage of progression of the disease, small perivascular foci of demyelination merge, proliferates of microglial cells appear, the cells are loaded with lipids. As a result, plaques are formed that are devoid of oligodendrite. During the period of exacerbation, fresh foci of demyelination appear against the background of old foci. The death of such patients, as a rule, comes from pneumonia. 4. Encephalitis Encephalitis is inflammation of the brain associated with infection, intoxication, or trauma. Infectious encephalitis is caused by viruses, bacteria and fungi. 1. Viral encephalitis occurs as a result of a viral infection (arbovirus, herpes virus, enterovirus, cytomegalovirus, rabies virus, etc.). The course of the disease can be acute, subacute and chronic. Etiological diagnosis consists in conducting serological tests. Pathological anatomy Mononuclear inflammation of lymphocytes, plasma cells, and macrophages is characteristic. Diffuse proliferation of microglia and oligodendroglia with the formation of rod-shaped and amoeboid cells. Neurophagia is characteristic with the formation of neurophagic nodules, as well as intranuclear and intraplasmic inclusions. 2. Tick-borne encephalitis is an acute viral natural focal disease with transmissible or alimentary transmission. It is caused by the tick-borne encephalitis virus, which belongs to the arboviruses. The disease is seasonal. The incubation period is 7-20 days. The disease begins acutely with fever, severe headache, impaired consciousness, epileptic seizures, meningeal symptoms, paresis and paralysis are sometimes possible. Macroscopically marked hyperemia of cerebral vessels, swelling of its tissue and small hemorrhages. Microscopically noted (in the acute form) is the predominance of circulatory disorders and an inflammatory exudative reaction; perivascular infiltrates and neuronophagia often occur. With a protracted course, the proliferative reaction of glia and focal destruction of the nervous system predominate. The chronic course of encephalitis is characterized by fibrillar gliosis, demyelination, and sometimes atrophy of certain parts of the brain. LECTURE No. 20. Infectious diseases Infectious diseases are called diseases caused by infectious agents - viruses, bacteria, fungi. The infectious process depends on the state of the macroorganism, the immune system, on the nature of the interaction of the macro- and microorganism, on the characteristics of the microorganism, etc. The coexistence of macro- and microorganisms is of three types. 1. Symbiosis - micro and macroorganism coexist in the interests of each. 2. Commensalism - micro- and macroorganism do not influence each other. 3. Parasitism - the life of a microbe at the expense of a macroorganism. The infection can be exogenous, when the pathogen penetrates through the entrance gate, and endogenous (autoinfection), when its own microflora is activated. Classification According to the biological factor: 1) anthroponoses - infectious diseases that occur only in humans; 2) anthropozoonoses - infectious diseases of both humans and animals; 3) biocenoses are a group of anthroponoses and anthropozoonoses transmitted through insect bites. Etiologically: 1) viral infections; 2) rickettsiosis; 3) bacterial infections; 4) fungal infections; 5) protozoal infections; 6) parasitic infections. Transfer mechanism: 1) intestinal infections; 2) respiratory infections; 3) transmissible or blood infections; 4) infections of the outer integument; 5) infections with a different mechanism of transmission. According to the nature of clinical and anatomical manifestations, infections with a primary lesion are distinguished: 1) skin, fiber and muscles; 2) respiratory tract; 3) digestive tract; 4) nervous system; 5) cardiovascular system; 6) circulatory system; 7) urinary tract. According to the nature of the course, acute, chronic, latent (hidden) and slow infections are distinguished. 1. Viral diseases Viral infections represent one of the numerous groups of infectious diseases, diverse in clinical course and morphology; are highly contagious and capable of causing epidemics and pandemics. During the introduction or activation of the virus in the human body, various variants of morphological and functional changes can be observed. These include: 1) cytolytic effect of the virus (influenza, viral hepatitis A); 2) integration of the virus with the cell genome without its pronounced destruction (viral hepatitis B); 3) proliferation of target cells (parainfluenza, smallpox); 4) giant cell transformation (measles, respiratory syncytial infection); 5) formation of inclusion bodies (influenza, adenovirus infection, rabies). Some viruses can lead to neoplastic transformation of human cells. For example, Epstein-Barr virus is involved in the development of Burkitt's lymphoma and nasopharyngeal cancer, and T-lymphotropic virus type I (HTLV-I) in the development of T-cell lymphoma. However: most often, dystrophic changes or necrosis occur in cells, in some cases, peculiar cellular transformations with the formation of intracellular inclusions that are important in the morphological diagnosis of certain viral diseases. The formation of inclusions most often occurs in viral and chlamydial infections. They are detected by light microscopy and are rough indirect evidence of infection; may consist of either assembled viral particles or viral nucleic acid residues. Inclusions can form in the nucleus and cytoplasm of the cell. All viral infections are characterized by: 1) infiltration with mononuclear cells, i.e., lymphocytes, plasma cells and macrophages; most often infiltrates are located along the vessels, but sometimes they can spread to the parenchyma; 2) cell lysis (with cytolytic viral infections) and phagocytosis of cell debris by macrophages; when neurons are damaged, this process is called neuronophagy; 3) the formation of inclusions, which are often found in affected neurons and glial cells; 4) reactive hypertrophy and hyperplasia of astrocytes and microglial cells, often with the formation of groups of cells; 5) vasogenic edema. Flu Influenza is caused by influenza viruses and is an acute respiratory illness. anthropozoonotic disease. Pathological changes depend on the severity of the course of the disease. In a mild form of influenza, the mucous membrane of the upper respiratory tract is affected, where acute catarrhal rhinolaryngitis develops. The mucous membrane becomes swollen, hyperemic, with excessive serous-mucous discharge. Microscopically, against the background of plethora, edema and lymphoid cell infiltration of the subepithelial layer, hydropic dystrophy of ciliated epithelium cells and loss of cilia are noted. The secretory activity of goblet cells and serous-mucous glands increases, many epithelial cells are desquamated. The cytoplasm is characterized by the presence of epithelial cells of basophilic and oxyphilic inclusions. With a moderate severity of the course of the disease, the mucous membrane of not only the upper respiratory tract, but also the small bronchi, bronchioles and lung parenchyma is included in the pathological process. Serous-hemorrhagic inflammation develops in the trachea and bronchi, sometimes with foci of mucosal necrosis. Epithelial cells exfoliate and fill the lumen of the bronchi, which leads to the formation of foci of atelectasis and acute emphysema. Against the background of the latter, foci of influenza pneumonia can form. Serous exudate, alveolar macrophages, desquamated cells of the alveolar epithelium, erythrocytes, and neutrophils accumulate in the alveoli. The interalveolar septa are thickened due to proliferation of septal cells and infiltration by lymphoid cells. The severe form of the flu has 2 varieties. With influenza with severe general intoxication, serous-hemorrhagic inflammation and necrosis occurs in the trachea and bronchi. In the lungs, against the background of circulatory disorders and massive hemorrhages, there are multiple small foci of serous hemorrhagic pneumonia, which alternate with foci of acute emphysema and atelectasis. Hemorrhages can appear in the brain, internal organs, serous and mucous membranes, skin. Severe influenza with pulmonary complications is due to the addition of a secondary infection. There is fibrinous-hemorrhagic inflammation with extensive areas of necrosis in the mucous membrane and the formation of ulcers. Destructive panbronchitis develops, which leads to the formation of acute bronchiectasis, atelectasis foci and acute pulmonary emphysema. In the internal organs, a combination of dystrophic and inflammatory processes occurs. AIDS AIDS (acquired immunodeficiency syndrome) is a disease caused by the human immunodeficiency virus. There is a total suppression of the immune system, accompanied by the development of opportunistic infections (opportunistic low-virulence infection) and tumors (Kaposi's sarcoma, malignant lymphomas). HIV belongs to the group of retroviruses that have reverse transcriptase in the structure of vibrios - an enzyme that synthesizes DNA on the RNA template of the virus. Currently, we can talk about the existence of (at least) 3 genotypes of the causative agent of human immunodeficiency: HIV-1, HIV-2 and HTLV-4. Of these, HIV-1 is the most common. Pathological anatomy. There is a change in the lymph nodes in the form of follicular hyperplasia, and then is replaced by depletion of the lymphoid tissue. HIV encephalitis develops, which is characterized by pathological processes in the white matter and subcortical nodes of the brain. Foci of softening and vacuolization of white matter are determined; due to demyelination, it becomes a grayish tint. Opportunistic infections are characterized by a severe course, which is generalized and resistant to ongoing therapy. Opportunistic infections can be caused by protozoa (pneumocysts, toxoplasmosis, cryptosporidium), fungi (Candida genus, cryptococci), viruses (cytomegaloviruses, herpetic viruses) and bacteria (legionella, salmonella). Kaposi's sarcoma (multiple idiopathic hemorrhagic sarcoma) is manifested by purple-red spots, plaques and nodes located on the skin of the distal lower extremities with ulceration. Possible involution with the formation of scars and depigmented spots. Microscopically, the tumor consists of many newly formed chaotically located thin-walled vessels with a well-defined endothelium and bundles of spindle-shaped cells. In the loose stroma, hemorrhages and accumulations of hemosiderin are visible. Malignant lymphomas in AIDS predominantly have a β-cell structure. Burkitt's lymphoma is common. 2. Diseases caused by bacteria Typhoid fever Typhoid fever is an acute infectious disease from the group of anthroponoses. The causative agent is typhoid bacillus. The incubation period is 10-14 days. The coincidence of the clinical cycles of the course of typhoid fever with certain cycles of anatomical changes in the lymphatic formations of the intestine served as the basis for constructing a scheme of morphological changes by stages. At the first stage of morphological changes, which usually coincides with the 1st week of the disease, in the lymphatic apparatus of the intestines, a picture of the so-called brain-shaped swelling is observed - an inflammatory infiltration of Peyer's plaques and solitary follicles. In the second stage, corresponding to the 2nd week of the disease, necrosis of the swollen Peyer's patches and solitary follicles occurs (the necrosis stage). Necrosis usually captures only the surface layers of the lymphatic apparatus of the intestine, but sometimes it can reach the muscular and even the serous membrane. In the third stage (the period of ulcer formation), approximately corresponding to the 3rd week of the disease, the dead areas of Peyer's patches and solitary follicles are rejected and ulcers form. This period is dangerous with possible severe complications (intestinal bleeding, perforation). The fourth stage (the period of pure ulcers) corresponds to the end of the 3rd and 4th weeks of the disease; in this period, the bottom of the typhoid ulcer becomes wide, it is cleared and covered with a thin layer of granulation tissue. The next phase (the period of ulcer healing) is characterized by the process of ulcer healing and corresponds to the 5-6th week of the disease. Morphological changes can spread to the large intestine, gallbladder, liver. At the same time, ulcers characteristic of typhoid fever are found on the mucous membrane of the gallbladder, and typhoid granulomas are found in the liver; the disease proceeds with symptoms of damage to these organs (jaundice, acholic stools, elevated blood levels of bilirubin, etc.). Damage to the intestines in typhoid and paratyphoid is always combined with damage to the regional lymphatic glands of the mesentery, and often the retroperitoneal glands. Under microscopy, the same macrophage reaction is noted in them, as in the lymphatic apparatus of the intestinal wall. In the enlarged lymph nodes of the mesentery, foci of necrosis are observed, in some cases, capturing not only the main mass of the lymph node, but also passing to the anterior sheet of the abdominal integument, which can cause a picture of mesenteric-perforative peritonitis. Other lymph nodes can also be affected - bronchial, paratracheal, mediastinal. The spleen in typhoid fever is enlarged as a result of blood filling and inflammatory proliferation of reticular cells with the formation of specific granules. The liver is swollen, soft, dull, yellowish on the cut, which is associated with the severity of parenchymal degeneration. In the kidneys, a cloudy swelling is found, sometimes necrotic nephrosis, less often hemorrhagic or embolic nephritis; frequent inflammatory processes in the urinary tract. In the bone marrow, areas of hemorrhage, typhoid granulomas, and sometimes necrotic foci appear. There are degenerative changes in the heart muscle. Pathological changes in the lungs in typhoid-paratyphoid diseases are in most cases inflammatory. Hyperemia of the meninges and edema of the substance of the brain are found. salmonellosis Salmonellosis is an intestinal infection caused by salmonella; refers to anthropozoonoses. Pathological anatomy With the most common gastrointestinal form of salmonellosis, the presence of edema, hyperemia, small hemorrhages and ulcerations in the mucosa of the gastrointestinal tract is macroscopically detected. Histologically, there are: excessive secretion of mucus and desquamation of the epithelium, superficial necrosis of the mucous membrane, vascular disorders, nonspecific cellular infiltration, etc. In addition to these changes, in severe and septic forms of the disease, signs of dystrophy and foci of necrosis in the liver, kidneys and other organs are often observed . The reverse development of morphological changes in most patients occurs by the 3rd week of illness. Dysentery Dysentery is an acute intestinal infectious disease with a predominant lesion of the large intestine and intoxication phenomena. Macroscopically, the intestinal lumen contains semi-liquid or mushy masses with an admixture of mucus and sometimes with streaks of blood. The intestine is slightly elongated in places, spasmodic in other areas. The mucous membrane is swollen, unevenly full-blooded, covered with large flakes of mucus or more evenly distributed and less viscous contents. After its elimination, small hemorrhages and shallow ulcerations at the tops of the folds are distinguishable. Lymph nodes of the mesentery grow in size, become reddish. All changes are focal in nature. Cholera Cholera is an acute infectious disease (anthroponosis) with a primary lesion of the stomach and small intestine. The causative agents are Koch's Asian cholera vibrio and El Tor vibrio. The pathological anatomy of cholera consists of local and general changes. Local transformations are formed (mainly) in the small intestine. The first 3-4 days are designated as the algid (cold) stage of cholera. The mucous membrane of the small intestine is full-blooded, edematous, with small hemorrhages throughout. Microscopically visible desquamation of the epithelium of the villi. Many vibrios are found in the intestinal wall. In general, the changes correspond to the picture of the most acute serous or serous-desquamative enteritis. The lymph nodes of the mesentery are somewhat enlarged. The peritoneum is plethoric, dry, with petechial hemorrhages. It is typical for the appearance of sticky plaque on it and between the loops of the small intestine, stretching in the form of threads, consisting of strands of desquamated mesothelium. Dense dark red blood in blood vessels, cavities of the heart, on sections of parenchymal organs. The serous membranes are dry, covered with sticky mucus, stretching in the form of threads. Dry full-blooded peritoneum with pinpoint hemorrhages and its inherent sticky coating between the loops of the small intestine, consisting of strands of desquamated mesothelium. The spleen is reduced, the follicles are atrophic, the capsule is wrinkled. In the liver, dystrophic processes develop in hepatocytes, foci of necrosis are formed in the parenchyma. Bile formation is disturbed. The gallbladder is enlarged in size, filled with transparent light bile - "white bile". The kidney acquires a characteristic appearance (the so-called motley kidney) - the cortical layer swells, pale, and the pyramids are filled with blood and acquire a cyanotic hue. As a result of anemia of the cortex, severe dystrophy develops in the epithelium of the convoluted tubules, leading to necrosis, which can contribute to oliguria, anuria and uremia. The loops of the small intestine are stretched, in its lumen there is a large amount (3-4 l) of a colorless liquid that is odorless, reminiscent of "rice water", without admixture of bile and the smell of feces, sometimes similar to "meat slops". In the liquid there are a large number of cholera vibrios. Microscopically, during the algidic period in the small intestine, there is a sharp plethora, swelling of the mucous membrane, necrosis and desquamation of epithelial cells - villi, resembling "faded dandelion heads" (N. I. Pirogov). In the mucous and submucosal layer - cholera vibrios in the form of "flocks of fish". There is hyperplasia of solitary follicles and Peyer's patches. In the striated muscles, foci of waxy necrosis sometimes occur. In the brain and spinal cord, in the cells of the sympathetic nodes, dystrophic, sometimes inflammatory phenomena occur; there may be hemorrhages in the brain tissue. Nisslev granularity, swollen and partially subjected to degranulation, is noted in many cells; hyalinosis of small vessels, especially venules, is noted. Plague Plague is an acute infectious disease caused by the plague bacillus. There are bubonic, skin-bubonic (skin), primary pulmonary and primary septic forms of plague: 1) bubonic plague is characterized by an increase in regional lymph nodes, usually inguinal, less often - axillary and cervical. Such lymph nodes are called primary plague buboes of the 1st order. They are enlarged, soldered, testate, immobile, dark red in color with foci of necrosis. Edema develops around the bubo. Microscopically, a picture of acute serous-hemorrhagic lymphadenitis is observed, a mass of microbes accumulates in the tissue. Proliferation of reticular cells is characteristic. With the formation of foci of necrosis, lymphadenitis acquires a hemorrhagic-necrotic character. Due to the development of necrosis, purulent inflammation and melting of the lymph node tissue occur, ulcers are formed, which, with a favorable result, are scarred. With the lymphogenous spread of the infection, new buboes appear (primary buboes of the 2nd, 3rd order, etc.), where the same morphological changes are observed as in the regional lymph node. Hematogenous development of infection leads to the rapid development of plague bacteremia and septicemia, which are manifested by rash, multiple hemorrhages, hematogenous lesions of the lymph nodes, spleen, secondary plague pneumonia, dystrophy and necrosis of parenchymal organs. The rash may take the form of pustules, papules, erythema, with the obligatory formation of hemorrhages, necrosis and ulcers. Multiple hemorrhages are observed in the serous and mucous membranes. With hematogenous lesions of the lymph nodes, secondary buboes appear (serous-hemorrhagic, hemorrhagic-necrotic lymphadenitis). The spleen is enlarged 2-4 times, septic, flabby, foci of necrosis are formed, a leukocyte reaction to necrosis is observed. Secondary pneumonia, which occurs as a result of hematogenous infection, has a focal character. A large number of dark red foci with areas of necrosis is a serous-hemorrhagic inflammation, where many pathogens are found. In parenchymal organs, dystrophic and necrotic changes can be observed; 2) the skin-bubonic (skin) form of the plague differs from the bubonic one in that the primary affect occurs at the site of infection. It is represented by a "plague conflict" (a vial with serous-hemorrhagic contents), or a plague hemorrhagic carbuncle. Lymphangitis is found between the primary affect and the bubo. At the site of the carbuncle, edema is noted, thickening of the skin, which becomes dark red; 3) primary pneumonic plague is extremely contagious. With primary pneumonic plague, lobar pleuropneumonia occurs. Pleurisy serous-hemorrhagic. At the very beginning of the disease, with the existing plethora of lung tissue, foci of serous-hemorrhagic inflammation are formed. During the development of the disease, stasis, hemorrhages, foci of necrosis and secondary suppuration are formed. Multiple hemorrhages in the internal organs; 4) primary septic plague is characterized by a picture of sepsis without visible entry gates of infection with a very severe course. Significantly expressed hemorrhagic syndrome (hemorrhage in the skin, mucous membranes, internal organs). anthrax Anthrax is an acute infectious disease characterized by a severe course in which skin and internal organs are affected; belongs to the group of anthropozoonoses. The causative agent of anthrax is an immobile bacterium Bacterium anthracis, which forms highly resistant spores: they remain in water and soil for decades. There are the following clinical and anatomical forms of anthrax: 1) skin (conjunctival, as a kind of skin); 2) intestinal; 3) primary pulmonary; 4) primary septic. The cutaneous form is very common. Morphologically, it manifests itself as an anthrax carbuncle. It is based on serous-hemorrhagic inflammation. Practically together with a carbuncle, regional serous-hemorrhagic lymphadenitis occurs. Lymph nodes are significantly enlarged, dark red on section. There is a sharp plethora, edema and hemorrhage in the tissue, in which a large accumulation of microbes is found. Loose tissue near the lymph nodes is edematous, with areas of hemorrhage. Most often, the outcome of the skin form is recovery, but in 25% of cases, sepsis develops. The conjunctival form, as one of the types of skin, develops when spores enter the conjunctiva and is characterized by serous-hemorrhagic ophthalmitis, swelling of the tissue around the eyes. In the intestinal form of the disease, extensive areas of hemorrhagic infiltration and ulcers form in the lower ileum, and serous hemorrhagic ileitis is formed. In the lymph nodes of the mesentery, regional serous-hemorrhagic lymphadenitis occurs. The intestinal form is most often complicated by sepsis. The primary pulmonary form is characterized by hemorrhagic tracheitis, bronchitis and serous-hemorrhagic focal or confluent pneumonia. The lymph nodes of the roots of the lungs swell, increase, foci of hemorrhages are observed, which is associated with serous-hemorrhagic inflammation. The primary pulmonary form is often complicated by sepsis. The primary septic form is characterized by general manifestations of infection in the absence of local disorders. General manifestations are the same both in primary sepsis and in secondary, complicating skin, intestinal or primary pulmonary forms of the disease. The spleen is enlarged and flabby, dark cherry in color, almost black on the cut, gives abundant scraping of the pulp. Hemorrhagic meningoencephalitis develops. The soft membranes of the brain are edematous, saturated with blood, have a dark red color ("red cap" or "cardinal's cap"). Microscopically, there is a serous-hemorrhagic inflammation of the membranes and tissue of the brain with a characteristic destruction of the walls of small vessels, their rupture, and the accumulation of a huge number of microbes in the lumen of the vessels. Tuberculosis Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis. Pathologically, there are 3 main types: 1) primary tuberculosis; 2) hematogenous tuberculosis; 3) secondary tuberculosis. The classical form of the morphological manifestation of primary tuberculosis is the primary tuberculosis complex. In 90% of cases, the foci of the formation of the primary tuberculosis complex are the upper and middle sections of the lungs, but it is also possible in the small intestine, bones, etc. In the primary pulmonary affect, alveolitis develops, which is quickly replaced by the typical development of cheesy necrosis. In the center of the primary affect, caseosis is formed, along the periphery - elements of nonspecific inflammation. The primary pulmonary focus is most often located directly under the pleura, so the pleura is often involved in a specific process. In the lymphatic vessels, expansion-infiltration of the walls and the appearance of tubercles occur. Elements of inflammation appear in the regional lymph nodes, turning into specific caseous changes with necrosis. Perifocal inflammation around the lymph nodes extends to the mediastinal tissue and adjacent lung tissue. In terms of the severity of the lesion, the process in the lymph nodes exceeds the changes in the area of primary affect, so reparative changes in the lymph nodes proceed more slowly. There are 4 phases of the course of primary pulmonary tuberculosis: 1) pneumonic; 2) resorption phase; 3) sealing phase; 4) formation of the center of Gon. In the first phase (pneumonic), the focus of broncholobular pneumonia (pulmonary affect) is determined in size from 1,5-2 to 5 cm. The shape of the pulmonary affect is round or irregular, the character is heterogeneous, the contours are blurred. At the same time, enlarged hilar lymph nodes are determined, an increase in the broncho-vascular pattern between the focus and the root of the lung - lymphangitis. In the second phase of resorption (bipolarity), a decrease in the zone of perifocal inflammation is observed, a centrally located caseous focus is more clearly revealed. Inflammatory changes in the regional lymph nodes in the region of the bronchopulmonary vessels are reduced. In the third phase (seals), the primary focus is well defined, its contours are clear, along the periphery of the focus, calcification in the form of small crumbs begins; marginal calcification is also present in the bronchopulmonary lymph nodes. In the fourth phase (formation of the Gon focus) at the site of the focus of broncholobular pneumonia, calcification becomes compact, the focus acquires a rounded shape and even clear contours, its size does not exceed 3-5 mm. Such a formation is called the focus of Gon. Outcomes of the primary tuberculosis complex: 1) healing with encapsulation, calcification or ossification; 2) progression with the development of various forms of generalization, the addition of nonspecific complications such as atelectasis, pneumosclerosis, etc. Hematogenous generalization develops when Mycobacterium tuberculosis enters the blood. A prerequisite for hematogenous generalization is the state of hyperergy. Depending on the state of the primary tuberculosis complex, early generalization is distinguished, which manifests itself in the form of: 1) generalized miliary tuberculosis with a massive rash of productive or exudative nodules in all organs; 2) focal tuberculosis with the formation of caseous foci up to 1 cm in diameter in different organs. Foci of hematogenous generalization can be a source of development of tuberculosis in various organs. With the progression of hematogenous disseminated tuberculosis, caverns are formed. Caverns are formed as a result of cheesy decay and melting of necrotic masses. In the hematogenous form of pulmonary tuberculosis, the cavities are thin-walled, multiple and are located symmetrically in both lungs. Damage to blood vessels, their thrombosis and obliteration play a role in the origin of such cavities. The nutrition of the affected areas of the lungs is disturbed and destruction is formed by the type of trophic ulcers. With the formation of caverns, the possibility of bronchogenic seeding of healthy areas of the lungs opens up. There are 7 forms of secondary tuberculosis: acute focal, fibrinose-focal, infiltrative, acute cavernous, cirrhotic tuberculosis, caseous pneumonia and tuberculoma. Sepsis Sepsis is a common infectious disease that occurs due to the existence of a focus of infection in the body. The main morphological features of sepsis are severe dystrophic and necrobiotic changes in the internal organs, inflammatory processes of varying severity in them, as well as a significant restructuring of the immune system. Sepsis has the most typical morphological picture with septicopyemia. As a rule, in all observations, a primary septic focus is clearly recorded, localized at the entrance gate. In the tissues of this focus there is a huge number of microbial bodies, intensive infiltration of leukocytes and areas of necrosis are recorded, signs of acute phlebitis or thrombophlebitis are determined. A characteristic sign of septicopyemia is the presence in many organs of metastatic purulent foci, which can often be detected with the naked eye. However, often these foci are found only under a microscope in the form of small foci, usually near blood or lymphatic vessels with symptoms of vasculitis. Another typical sign of septicopyemia is dystrophic and necrotic changes in the internal organs, the severity of which often depends on the duration of the disease. At the onset of the disease, hyperplastic manifestations predominate, which is accompanied by an increase in their size and an increase in the area of functional areas, and with a longer course of the disease, destructive processes are found in the organs of immunogenesis, accompanied by mass death of immunocompetent cells with almost complete depletion of all organs of the immune system. The most typical are changes in the spleen ("septic spleen"). It is enlarged, flabby, cherry-red in section. Another variant of sepsis - septicemia - is characterized by significant features. As a rule, a fulminant course is typical for this form of sepsis. The main morphological sign of septicemia is generalized vascular disorders: stasis, leukostasis, microthrombosis, hemorrhage. The primary septic focus at the entrance gate does not always have a clear picture and is often not detected (cryptogenic sepsis). Metastatic foci typical of septicopyemia are not detected, although in some cases small inflammatory infiltrates are recorded in the stroma of some organs. Characterized by severe destructive processes in parenchymal organs and hyperplastic changes in the organs of immunogenesis (in particular, "septic spleen"). However, the efficiency of the functioning of the immune system is low, and microscopic examination reveals a picture of incomplete phagocytosis. Septicemia is often considered in connection with bacterial (septic) shock, which is caused mainly by gram-negative flora and proceeds with severe microcirculation disorders, blood shunting. Deep ischemia of the internal organs, caused by vascular disorders, leads to necrotic processes in many organs (in particular, cortical necrosis of the kidneys, etc.). Pulmonary edema, hemorrhages and erosions in the gastrointestinal tract are typical. Patients with sepsis die from septic shock. Syphilis Syphilis, or lues, is a chronic infectious sexually transmitted disease caused by Treponema pallidum. Pale treponemas get on the skin or mucous membrane of a healthy person; through the existing microcracks in the stratum corneum, and sometimes through the intercellular gaps of the intact integumentary epithelium, there is a rapid penetration into the tissues. Pale treponema intensively multiply at the site of implementation, where, approximately a month after the incubation period, primary syphiloma (hard chancre) is formed - the first clinical manifestation of syphilis. At the same time, infectious agents enter the lymphatic clefts, where they multiply rapidly and begin to spread through the lymphatic vessels. Some infectious agents penetrate into the bloodstream and into the internal organs. Reproduction of pale treponemas and their promotion along the lymphatic pathways also occurs after the formation of primary syphiloma in the primary period of syphilis. At this time, there is a consistent increase in lymph nodes (regional adenitis), close to the entrance gate, and then more distant (polyadenitis). At the end of the primary period, pale treponemas that have multiplied in the lymphatic tract through the thoracic duct penetrate into the left subclavian vein and are carried by blood flow in large numbers to organs and tissues. The secondary period of syphilis occurs after 6-10 weeks and is characterized by the appearance of syphiloids - multiple inflammatory foci on the skin and mucous membranes. Depending on the intensity of inflammation and the predominance of exudative or necrobiotic processes, 3 types of syphiloids are distinguished: roseola, papules and pustules. They are rich in treponemes. After their healing, small scars remain. Tertiary syphilis develops after 3-6 years and is characterized by chronic diffuse interstitial inflammation that occurs in the lungs, liver, aortic wall and testicular tissue. Along the course of the vessels, a cellular infiltrate is observed, consisting of lymphoid and plasma cells. Gumma is a focus of syphilitic productive-necrotic inflammation, syphilitic granuloma; can be single or multiple. 3. Fungal diseases Fungal diseases (mycoses) are a group of diseases caused by fungi. With some mycoses, exogenous infection occurs (trichophenia, scab, actinomycosis, nocardiosis, coccidiomycosis), while with others it is exogenous, that is, autoinfection develops under the influence of adverse factors (candidiasis, aspergillosis, penicillosis, mucormycosis). There are fungal diseases of the skin (dermatomycosis) and internal organs (visceral mycoses). 1. Dermatomycosis is divided into 3 groups: epidermycosis, superficial and deep dermatomycosis: 1) epidermycoses are characterized by damage to the epidermis and are caused by epidermophytes of various types (pityriasis versicolor, epidermophytosis); 2) with superficial dermatomycosis, the main changes develop in the epidermis (trichophytosis and scab); 3) deep dermatomycoses are characterized by damage to the dermis itself, but the epidermis also suffers. 2. Visceral mycoses differ according to the etiological factor: 1) diseases caused by radiant fungi (actinomycosis, nocardiosis); 2) diseases caused by yeast-like and yeast fungi (candidiasis, blastomycosis); 3) diseases caused by mold fungi (aspergillosis, penicillosis, mucormycosis); 4) diseases caused by other fungi (coccidioidomycosis, rhinosporidiosis, sporotrichosis, histoplasmosis). Actinomycosis Actinomycosis is a visceral mycosis characterized by a chronic course, the formation of abscesses and granules. Caused by the anaerobic radiant fungus Actinomyces Israeli. Pathological anatomy When the fungus enters the tissue around it, hyperemia, stasis develops, neutrophils begin to emigrate, which leads to the formation of an abscess, around which macrophages, young connective tissue elements, plasma cells proliferate, xanthoma cells and newly formed vessels appear. An actinomycotic granuloma is formed. These granulomas are prone to fusion and the formation of dense foci, on the cut of a yellow-greenish color. White grains are visible in the pus - actinomycete drusen. Druses are represented by numerous short rod-shaped elements of the fungus, attached at one end to a homogeneous center, which is a conglomerate of intertwining mycelium. The disease proceeds for a long time, fistulas can occur, and the most severe complication is amyloidosis. Candidiasis Candidiasis, or thrush, is caused by yeast-like fungi of the genus Candida. This is an autoinfectious disease that occurs when exposed to adverse factors or when taking antibacterial drugs. It can occur locally (skin, mucous membranes, gastrointestinal tract, urinary organs, lungs, kidneys) and generalized. With local candidiasis, mucous membranes covered with stratified squamous epithelium are most often affected. The fungus grows superficially, brownish overlays appear, consisting of intertwining threads of pseudomycelium, desquamated epithelial cells and neutrophils. When the fungus penetrates into the thickness of the mucous membrane, foci of its necrosis appear. Necrotic areas are separated from healthy tissue by a demarcation shaft of neutrophils. The germination of pseudomycelium into the lumen of the vessel indicates metastasis. In the internal organs around the fungi, a neutrophilic infiltrate appears. With a prolonged course, granulomas are formed, which consist of macrophages, fibroblasts and giant multinucleated cells. With candidiasis of the esophagus, films are formed on the mucous membrane that completely cover the lumen. Injury to the stomach is rare. When the intestines are affected, ulcers and pseudomembranous overlays occur. With damage to the kidneys in the cortical layer, small pustules, foci of necrosis and granulomas appear, which contain elements of the fungus. Mushrooms can penetrate into the lumen of the tubules and be excreted in the urine. With candidiasis of the lungs, fibrinous inflammation is formed with necrosis in the center. In the future, suppuration and the formation of cavities occur. With a prolonged process, granulation tissue is formed; the process ends with fibrosis. Generalized candidiasis is characterized by the entry of fungi into the bloodstream and the appearance of metastatic foci (candidiasis septicopyemia). Aspergillosis Aspergillosis is caused by several species of the genus Aspergillus. As an autoinfection, it occurs when treated with high doses of antibiotics, steroid hormones and cytostatics. Pathological anatomy. The most typical pulmonary aspergillosis, which is divided into: 1) non-purulent pulmonary aspergillosis, in which gray-brown dense foci are formed with a whitish center, where a fungus accumulates among the infiltrate; 2) purulent pulmonary aspergillosis, in which foci of necrosis and suppuration are formed; 3) aspergillosis-mycetoma - characterized by the formation of a bronchiectasis or lung abscess; the pathogen grows along the inner surface of the cavity and forms thick wrinkled membranes that exfoliate into the lumen of the cavity; 4) tuberculoid pulmonary aspergillosis - characterized by the appearance of nodules similar to tubercular. 4. Diseases caused by protozoa Malaria Malaria is an acute or chronic relapsing infectious disease that has different clinical forms depending on the period of maturation of the pathogen, characterized by febrile paroxysms, hypochromic anemia, enlargement of the spleen and liver. The disease is caused by several species of protozoa of the genus Plasmodium. Once in the bloodstream with a mosquito bite, plasmodia go through a complex development cycle, parasitize in human erythrocytes, reproducing asexually (schizogony). Given the existence of several types of Plasmodium, three-day, four-day and tropical forms of malaria are distinguished. With three-day malaria, red blood cells are destroyed and anemia occurs. The products released during the breakdown of erythrocytes (hemomelanin) are captured by the cells of the macrophage system, which leads to an increase in the spleen and liver, bone marrow hyperplasia. The organs are filled with pigment and become dark gray, and sometimes black. The spleen is enlarged and plethoric. Subsequently, hyperplasia of cells occurs that phagocytize the pigment. The pulp becomes dark. In chronic course, the spleen is compacted due to sclerotic processes, on a gray-black incision; its mass can reach 3-5 kg. The liver is enlarged, plethoric, gray-black. The stellate reticuloendotheliocytes are hyperplastic and contain hemomelanin. In a chronic course, the stroma of the liver is rough and the proliferation of connective tissue is characteristic. The bone marrow of flat and tubular bones has a dark gray color, the cells are hyperplastic with the presence of pigment. Hemomelanosis of the organs of the histiocytic-macrophage system is combined with hemosiderosis. Hepatic jaundice develops. The pathological anatomy of a four-day malaria is similar to a three-day one. Tropical malaria differs from other species in that erythrocytes containing schizonts accumulate in the terminal sections of the bloodstream, where they develop. At the same time, numerous petechial hemorrhages occur in the cerebral cortex and other parts of the gray matter, which surround the vessels filled with agglutinated erythrocytes with parasites. Around such vessels, foci of necrosis of the brain tissue also appear. The brain acquires a brown-gray (smoky) color. On the border of necrosis and hemorrhage, after 2 days, a reactive proliferation of cells appears and the formation of peculiar nodules - specific Durk. The death of such patients is typical for tropical malaria, which is complicated by coma. Amoebiasis Amoebiasis, or amoebic dysentery, is a chronic protozoal disease, which is based on chronic recurrent ulcerative colitis. Called by the protozoa of the class of rhizopods - Entamoeba histolitica. Getting into the wall of the colon, the amoeba and its metabolic products cause edema and histolysis, necrosis of the mucous membrane, and the formation of ulcers. Necrotic-ulcerative changes are most often localized in the caecum. Microscopically, areas of mucosal necrosis are swollen and stained dirty gray or greenish. The zone of necrosis penetrates deep into the submucosal and muscular layers. With the formation of an ulcer, its edges become undermined and hang over the bottom. Amoebas are located on the border between necrotic and preserved tissue. A secondary infection can join - then an infiltrate from neutrophils occurs and pus appears. A phlegmonous, or gangrenous, form of colitis is formed. Deep ulcers heal with a scar. Lymph nodes are enlarged, but there are no amoebas in them. Complications can be intestinal and extraintestinal. Of the intestinal, the most dangerous are perforated ulcers, accompanied by bleeding, the formation of stenosing scars after the healing of ulcers, and the development of inflammatory infiltrates around the affected intestine. Of the extraintestinal complications, the most dangerous is a liver abscess. Author: Kolesnikova M.A.
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