LECTURE No. 10 Topographic anatomy and operative surgery of the pelvic organs Under the "pelvis" in descriptive anatomy is meant that part of it, which is called the small pelvis and is limited to the corresponding parts of the ilium, ischium, pubic bones, as well as the sacrum

LECTURE No. 11 Topographic anatomy and purulent surgery Purulent-septic diseases or complications are observed in about a third of the total surgical contingent of patients;

ETIOLOGY, PATHOGENESIS, PATHOLOGICAL ANATOMY The etiopathogenesis of mental disorders in AIDS is associated with two factors: 1) general intoxication and increasing damage to brain neurons; 2) mental stress that develops after receiving news of the presence

Etiopathogenesis, pathological anatomy A single cause of anorexia nervosa and bulimia nervosa has not been established. Various factors are involved in the etiopathogenesis of the disease. An important role is played by the predisposition of the personality (premorbid accentuations), family

11. PATHOLOGICAL ANATOMY 11.1. Possible pathoanatomical changes in men About pathoanatomical changes in the genital organs in men, as a consequence of onanism, we can talk insofar as the inflammatory processes caused by onanism in

6.4. PATHOLOGICAL ANATOMY OF DENTAL CARIES In the clinical course of caries, two stages are distinguished: the first is characterized by a change in color and, apparently, of the undamaged surface of the enamel, the second is the formation of a tissue defect (carious cavity). The second stage is quite complete

Test

on pathological anatomy of farm animals

Completed:

Correspondence student

4th year, group I, code-94111

Altukhov M.A. IV option

Checked_________________

Omsk 1998
TOC o "1-3"

PROTEIN DYSTROPHIES (DYSPROTEINOSIS)____________________________ PAGEREF _Toc415965939 h 3

Tick-borne Encephalitis _______________________________________________ PAGEREF _Toc415965940 h 5

DIPLOCOCCAL SEPTICYMIA _______________________________________ PAGEREF _Toc415965941 h 7

References __________________________________________________ PAGEREF _Toc415965942 h 9

PROTEIN DYSTROPHY (DYSPROTEINOSIS)

DYSTROPHY (from dys... and Greek trophe - nutrition), a pathological process of replacing the normal components of the cytoplasm with various ballast (or harmful) products of metabolic disorders or their deposition in the intercellular space. There are protein, fat, carbohydrate and mineral dystrophies. In a broader sense, dystrophy is also called any biochemical disorders in tissues (eg, myocardial dystrophy) or nutritional disorders.

Proteins play a major role in life processes. They are divided into simple and complex. The most important simple proteins are proteins: albumins and globulins; complex proteins - proteids: nucleoproteins, glucoproteins, chromoproteins, etc. The chemistry of protein metabolism in tissues in normal and pathological conditions has not yet been studied enough, therefore there is no rational classification of protein dystrophy.

The essence of protein dystrophies is that the structure of the cytoplasm of cells and intercellular substance is disturbed as a result of physicochemical changes in proteins, due to the redistribution of the amount of water in the tissues, the entry of protein substances foreign to the body brought by the blood into the tissues, an increase in cellular secretion, etc.

Depending on the predominant localization of morphological changes, dysproteinosis is usually divided into cellular, extracellular and mixed. By distribution, they can be general and local.

Cellular dysproteinoses include granular, hyaline-droplet, hydropic and horny dystrophy; to extracellular - hyalinosis and amyloidosis; to mixed - a violation of the exchange of nucleoproteins and glucoproteins.

Cellular dysproteinoses. Granular dystrophy - the appearance in the cytoplasm of grains and drops of a protein nature. The most common of all types of protein dystrophies. Parenchymal organs (kidneys, liver, myocardium) are involved in the dystrophic process, less often skeletal muscles. In this regard, granular dystrophy is called parenchymal dystrophy.

Under the microscope, swelling of the epithelial cells of the kidneys, liver and muscle fibers is noted, as well as the formation of granularity in their cytoplasm, which causes a cloudy appearance of the cells.

The appearance of granularity may be associated with swelling and rounding of mitochondria under conditions of tissue hypoxia or is the result of decomposition of protein-lipoid complexes of the cytoplasm, pathological transformation of carbohydrates and fats into proteins, denaturation of cellular protein, or infiltration of cells with proteins foreign to the body brought with blood flow.

Macroscopically, organs with granular dystrophy are swollen, flabby in consistency. They are painted paler than normal, due to squeezing of the capillaries by swollen cells. When cut, the parenchyma swells, dull appearance, the pattern is smoothed. The heart muscle resembles meat scalded with boiling water, and the liver and kidneys are gray-brown in color.

The cause of granular dystrophy can be infectious diseases, various intoxications of the body, circulatory disorders and other factors leading to the accumulation of acidic products in the tissues.

Clinical significance: granular dystrophy can cause dysfunction of the affected organs, especially important ones such as the heart - the contractility of the myocardium is weakened.

Hyaline-drop dystorphia - the appearance in the cytoplasm of large translucent homogeneous protein drops. This process is based on the resorption of pathological protein substances (paraproteins) by the cells when they appear in the plasma, or hyaline-like drops are formed due to the denaturation of their own cellular proteins. This dystrophy is noted in foci of chronic inflammation of tissues, glandular tumors, but especially often in the epithelium of the renal tubules with nephrosis and nephritis. During life, in animals with nephritis, protein and casts are found in the urine.

The outcome of hyaline-drop dystorphy is unfavorable, since this process turns into necrosis.

Hydroscopic (hydroscopic, vacuolar) dystrophy - the formation in the cytoplasm of cells of various sizes of vacuoles with a transparent liquid. With the development of the process, karyolysis occurs and the cell turns into a large vesicle filled with liquid, poor in elk and therefore not perceiving histological colors ("balloon dystorophia"). The essence of this dystrophy is the change in colloid osmotic pressure and increased permeability of cell membranes. It is observed in the cells of the epidermis of the skin with the development of edema, an infectious lesion of the skin (for example, with smallpox, foot and mouth disease); in the liver, kidneys, adrenal glands, muscle fibers, nerve cells and leukocytes - with septic diseases, intoxications, debilitating conditions of the body, etc.

Vacuolar dystrophy is determined only under a microscope. Vacuolization of the cytoplasm, which is not related to hydropic dystrophy, is observed in the ganglia of the central and peripheral nervous system, as a manifestation of physiological secretory activity. Signs of vacuolization can be detected postmortem in tissues and organs containing large amounts of shcolene (liver, muscle tissue, nerve cells). This is due to the fact that in the corpse, under the action of enzymatic processes, glycolen is broken down, as a result of which vacuoles are formed in the cytoplasm. In addition to vacuolization of the cytoplasm, signs of cloudy swelling are also characteristic.

Vacuolar degeneration should not be confused with fatty degeneration, since in the process of manufacturing histological preparations using solvents (alcohol, xylene, chloroform), fatty substances are removed and vacuoles appear in their place. To differentiate these dystrophies, it is necessary to prepare sections on a freezing microtome and stain them for fat.

The outcome of hydropic dystophia is in most cases unfavorable, since cells die during this process.

Horny dystrophy (pathological keratinization) - the formation of a horny substance (keratin) in the cells. Normally, keratinization processes are observed in the epidermis. Under pathological conditions, it may have excessive horn formation (hyperkeratosis) and a qualitative violation of horn formation (parakeratosis). Cornification occurs in the mucous membranes (leukoplakia).

Examples of hyperkeratosis are dry calluses that develop from prolonged skin irritation. Under the microscope, a thickening of the epidermis is noted due to excessive layering of the horny substance and hyperplasia of the cells of the Malpighian layer. The horny substance is stained pink with eosin, and yellow with Van Gieson's picrofuchin mixture. Occasionally, horses with inflammatory skin diseases develop a spiky thickening of the epidermis due to hypertrophy of the spiky cell layer and elongation of the interpapillary epithelial processes. Such lesions are called acanthosis (Greek akantha - thorn, needle). Hyperkeratosis includes the so-called ichthyosis (Greek ichtys - fish), which is a deformity. The skin of newborns in these cases is rough, hard due to the appearance of gray horny formations on it, like fish scales. Animals with such skin lesions usually die in the first days of life.

Excess horn formation is seen in warts, cancroid (a cancer-like tumor), and dermoid cysts.

Parakeratosis (Greek para - about, keratis - horny substance) - a violation of horn formation, expressed in the loss of the ability of epidermal cells to produce keratohyalin. In this condition, the stratum corneum is thickened, loose, and scales form on the surface of the skin. Under the microscope, discomplexed horny cells with rod-shaped nuclei are noted. Parakeratosis is observed in dermatitis and lichen lichen.

Leukoplakia is a pathological keratinization of the mucous membranes, arising from the action of various irritants, with inflammatory processes and beriberi A. It occurs, for example, in pigs on the mucous membrane of the prepuce from chronic irritation with urine. On the mucosa, whitish-gray raised areas of various sizes are formed, rounded in shape, consisting of keratinized epithelium. Sometimes this phenomenon is observed in the urethra, bladder and rumen of ruminants. With avitaminosis A, the glandular epithelium of the oral cavity, pharynx and esophagus becomes keratinized.

In morphological and pathogenetic terms, pathological keratinization is essentially not associated with a violation of protein metabolism, but is closer to the process of hypertrophic tissue growth and metaplasia.

Tick-borne Encephalitis

Encephalitis is an inflammation of the brain. Inflammatory processes in the brain must be distinguished from dystrophic changes in nerve cells and fibers (pseudoencephalitis or encephalomalacia) with the subsequent development of reactive processes that are observed in metabolic disorders and intoxications.

Classification of encephalitis. By origin, primary encephalitis (rabies, Borna's disease and others caused by neurotropic viruses) and secondary as a complication of the underlying disease (swine, dog and bird plague, malignant catarrhal fever, myt, etc.) are distinguished. According to the localization of the pathological process, encephalitis is divided into:

1) polioencephalitis (polios - gray) - inflammation, observed mainly in the gray matter of the cortex or brain stem (it is typical for rabies, Bornais disease, enzootic encephalitis of sheep and cattle, epidemic human encephalitis and some others);

2) leukoencephalitis - changes occur mainly in the form of demyelination of nerve fibers and growth of neuroglia in the white matter of the brain;

3) panencephalitis - simultaneous position of both white and gray matter of the brain (register it with swine, dog and bird plague, malignant catarrhal fever, carnivorous encephalitis, infectious encephalomyelitis of horses, etc.);

4) meningoencephalitis - the inflammatory process spreads from the meninges to the brain and spinal cord.

According to the prevalence of the inflammatory process, encephalitis is focal, disseminated and diffuse.

Depending on the different combination of components of the inflammatory reaction, the following are observed: acute non-purulent encephalitis of the lymphocytic type, serous encephalitis, purulent and hemorrhagic. Along the course, encephalitis can be acute, subacute and chronic.

The development of one form or another of encephalitis depends on the cause that causes it, the duration and strength of the pathogenic stimulus, and the reactive state of the organism itself. The clinical manifestation of encephalitis in its symptoms is diverse and depends on the localization and nature of the inflammatory process: increased irritability, attacks of violence, aggressiveness, depression, impaired motor functions, etc. Similar symptoms can also occur with inflammation of the meninges, which is important to take into account in pathomorphological studies.

Acute non-purulent encephalitis of the lymphocytic type is characteristic of a number of diseases caused by neurotropic or organotropic viruses (rabies, Borna disease of horses, enzootic encephalitis of sheep and cattle, rinderpest, plague of birds, pigs, dogs, malignant catarrhal fever of cattle, fox encephalitis, etc.). It also occurs as a complication of certain bacterial diseases and toxic effects. At the same time, in some cases, dystrophic changes in nerve cells, the reaction of glia (ectodermal forms of encephalitis) predominate, in others - vascular changes and reactive processes in the connective tissue (mesodermal forms of encephalitis).

Macroscopically, non-purulent encephalitis is not always recognizable, since the signs of an inflammatory reaction in the brain substance are not bright. In the most pronounced cases, with encephalitis, flabbiness of the medulla, uneven redness, some smoothness of the cerebral gyri of the cerebral hemispheres, as well as hemorrhages, hypermia and swelling of the meninges, an increase in the amount of fluid in the lateral ventricles, which sometimes becomes reddish, are noted.

Microscopically, alternative, exudative and proliferative processes are established in the brain tissue. Of the changes in the vascular connective tissue apparatus, the most significant is the presence of vascular and perivascular cellular infiltrates of hematogenous and local origin (multiplication of endothelial and adventitial cells of small vessels, veins, pre- and capillaries). As a result, cellular muffs are formed around the vessels, consisting mainly of small lymphoid cells, single rounded histiocytes, monocytes, and even less often plasma cells. Transitional cell forms occur between lymphoid cells and histiocytes, which indicates the genetic relationship of the cell proliferate. In some places, cellular infiltrates extend beyond the perivascular spaces and are distributed in the surrounding glial tissue of the brain.

Of other changes in the vascular network, plethora, lumen expansion, regional stasis, thrombosis, swelling, proliferation, desquamation of the endothelium, sometimes segmental necrosis and hyalnosis of the vascular walls, perivascular edema and hemorrhages should be noted. Sometimes in the cells of the infiltrate, karyopyknosis and karyorrhexis are noted.

Changes in glia are expressed by the multiplication of its cells and the appearance among them of degenerative forms (rod-like and fragmentation of nuclei, feathering). Proliferative processes on the part of glia are either focal or diffuse. At the same time, the polymorphism of its cells is noted, their transformation into wandering (mobile) forms. Glia proliferates are formed either around vessels or around nerve cells, and sometimes, independently of them, focal accumulations in the form of glial nodules are created. If the reproduction of glial cells takes place around nerve cells, then they speak of neuronophagy. Distinguish between true and false neuronophagy. True neuronophagy is considered to be one where the multiplication of glial cells occurs around the damaged nerve cell and only the cell glial nodule remains in place of the latter. False neuronophagy refers to the reproduction of the same elements of neuroglia around an intact nerve cell. In the chronic course of the disease (for example, with distemper), scars (gliosis, neuroglial sclerosis) can form from glial tissue.

Changes in nerve cells in encephalitis are diverse and are closely related to the nature and severity of the course of the process. The most important changes concern the chromatophilic, tigroid substance of the cytoplasm (Nissel grains). The process begins with swelling of the cytoplasm, combined with fine-grained, dusty disintegration of the Nissel grains up to their complete disappearance from the cell body (chromatolysis or tigrolysis). The essence of this process lies in the development of intracellular edema, which in the initial phases manifests itself in the form of partial chromatolysis either in the center of the nerve cell (perinuclear edema) or on the periphery (pericellular edema). Vacuoles often form in the marginal zone. Expressed forms of intracellular edema give the cytoplasm of the nerve cell the appearance of honeycombs. Electron microscopically note the disintegration of polysomes and ribosomes, vesiculation and expansion of the cistern of the endoplasmic reticulum, swelling and clearing of the mitochondrial matrix. The nuclei of nerve cells also undergo swelling, edema, and lysis. In the later stages, this process ends with complete lysis of the nerve cell (karyocytolysis).

In addition, changes in nerve cells are observed in the form of homogenization of the cytoplasm and nucleus, since the Nissel grains at the same time seem to merge into a homogeneous dark-colored mass (pyknosis or wrinkling of the nerve cell). The highest degree of such a process is defined as sclerosis of the nerve cell.

Neurofibrils can persist for a long time, but in most cases, along with changes in the chromatophilic substance, the neurofibrillary structure also changes. They form a finely looped network when sprayed with a tigroid substance or thicken unevenly, swell like varicose veins and break up into separate clumps and grains. Ultimately, they also undergo either hydrolytic melting (fibrillolysis) or fuse together and are more intensively impregnated with silver. In dystrophically altered nerve cells, myelin figures, drops of fat can be detected, and the pigment lipofuscin can accumulate. With complete dissolution of the tigroid substance, the neurofibrillary structure of the nerve cell usually completely disappears, which is revealed by silver impregnation or electron microscopy.

Along with the cytoplasm of nerve cells, changes in their nuclei are also noted: displacement of the nucleus to the periphery of the body of the nerve cell, swelling or wrinkling of it, change in shape (the nucleus acquires uneven contours), karyorrhexis, vacuolization and karyolysis. Sometimes the nucleolus shrinks, and it becomes like a mulberry. Nerve processes are also subject to dystrophic changes. They break down with the formation of detritus from myelin figures and fat droplets. In places of decay, mobile neuroglial cells appear, phagocytizing decay products and acquiring the appearance of granular balls. At the same time, along the course of the nerve processes, Schwann cells are usually activated, which are rounded, multiply with the formation of cell clusters. Then, in the intercellular substance of the nervous tissue, lytic processes begin to predominate, followed by softening of the brain, which is largely facilitated by serous exudation.

Dystrophic changes in nerve cells may be accompanied by structural changes that are compensatory and adaptive in nature, especially with a long course of the disease. These include hypertrophy of the nucleolus, nucleus and cells in general with hyperplasia of intracellular organelles, the appearance of binuclear cells, etc.

In many viral encephalitis, a specific process in nerve cells is the detection of inclusion bodies. These are acidophilic oval or round bodies with a certain internal structure. In some diseases, they are formed in the cytoplasm (rabies, plague, etc.), and in others, in the nuclei (enzootic encephalitis of horses, sheep, etc.). Inclusion bodies are formed as a product of the interaction of elementary bodies of the virus with nucleic acids and plasma proteins. Their nature and significance for the organism have not yet been studied enough, but they are of great diagnostic value.

Other forms of encephalitis (serous, hemorrhagic) are relatively rare in animals. Serous encephalitis of an infectious, toxic or allergic nature is manifested by swelling of the brain tissue. Hemorrhagic encephalitis is characterized, along with the changes mentioned above, by diapedesis of erythrocytes and their increased admixture to the inflammatory exudate. It is sometimes recorded in diseases caused by neurotropic viruses (Born's disease, etc.), swine fever, feed poisoning, botulism, etc. Macroscopically, individual or multiple foci of softening of a dark red or red-brown color are found, which differ from hemorrhages in that the hemorrhagic exudate does not coagulate. Histologically, they show strongly injected vessels, hemorrhagic exudate in the perivascular lymphatic spaces. Ganglion cells undergo necrobiosis and necrosis. Hemorrhagic encephalitis causes death very quickly.

DIPLOCOCCAL SEPTICYMIA

SEPSIS (from the Greek sepsis - putrefaction), a serious infectious disease that develops as a result of infection of the blood with microbes, mainly pyogenic (staphylococci, streptococci). It is expressed by a severe general condition, fever, clouding of consciousness, the formation of abscesses in the organs (septicopyemia), etc.

Diplococcal septicemia is a predominantly acute infectious disease of young animals, affecting more often calves and lambs, less often foals and piglets. Clinical and anatomically characterized by a picture of acute sepsis. The causative agent of the disease is diplococcus.

Pathogenesis - in natural conditions, infection occurs through the respiratory tract and the gastrointestinal tract. In places of primary introduction, diplococci multiply and subsequently penetrate into the lymphatic and blood tracts. With blood and lymph, the pathogen spreads through organs and tissues. Pathogen strains have toxinogenic properties, they secrete toxic products that suppress phagocytosis and increase the permeability of the vascular walls, which contributes to the hemolysis of red blood cells, the blood coagulation process is disturbed - toxemia develops with symptoms of hemorrhagic diathesis and severe organ damage.

pathological changes. In case of a hyperacute course of infection, at the autopsy of dead animals, multiple pinpoint and small-spotted hemorrhages are found on the mucous membrane of the small intestine, less often on the abomasum, on the mesentery, peritoneum, under the epicardium and endocardium. Acute hyperemia of the mucous membranes of the nasal cavity, larynx, trachea, severe hyperemia and serous pulmonary edema are also noted.

In an acute course, depending on the routes of infection and penetration of the pathogen into the body of the animal, the respiratory or digestive apparatus is predominantly affected.

When the respiratory apparatus is affected, conjunctival hyperemia, catarrhal inflammation of the mucous membrane of the upper respiratory tract, swelling and enlargement of bronchial lymph nodes, effusion into the chest cavity of serous or serous-hemorrhagic exudate, multiple petechial hemorrhages and fibrin deposits on the pleura, pericardium, serous-hemorrhagic or croupous pneumonia are noted. with a predominant lesion of the anterior and middle lobes, less often with coverage of the entire lung tissue; hemorrhages under the epi- and endocardium; dystrophic changes in the liver, kidneys and myocardium, enlargement of the spleen.

In cases where the infection occurs with a lesion of the gastrointestinal tract, hemorrhagic effusion is found in the abdominal cavity in large numbers; the spleen is sharply enlarged (2-3 times), rubber-like (rubber) consistency, with rounded edges, dotted and striped hemorrhages under the capsule. The liver is swollen, plethoric. Under the capsule of the kidneys, multiple small hemorrhages. More striking changes in the gastrointestinal tract; the mucous membrane of the abomasum and the small intestine is sharply hyperemic, in a state of serous edema, dotted with dotted and small-spotted hemorrhages; liquid contents in the intestinal cavity, in some cases painted red

(due to the admixture of blood). Similar signs, but weaker, are noted in the large intestine, especially in the blind and colon.

Mesenteric lymph nodes are strongly swollen, enlarged, gray-red in color, numerous petechial hemorrhages can be seen on the cut surface. Sometimes in the acute course of the disease, the respiratory organs and the gastrointestinal tract are simultaneously affected.

In chronic diplococcal infection, pathological changes are found mainly in the lungs. They are characterized by the development of fibrinous-necrotizing pneumonia, complicated by serous-fibrinous pleurisy and pericarditis, or they observe catarrhal-purulent pneumonia with the formation of multiple purulent foci of various sizes in the parenchyma of the organ, which subsequently undergo encapsulation. Joints are also often affected - serous-fibrinous or purulent inflammation of the articular bag and ulceration of the articular cartilage.

Diplococcal infection also occurs in adult animals (in cows, mares, sows and ewes), which are most often the source of infection for young animals (in utero, through milk, urine, nasal discharge). Pathological and anatomical changes in them are usually expressed in the development of catarrhal, catarrhal-purulent endometritis and mastitis.

The diagnosis of diplococcal septicemia in young animals, due to the absence of specific processes in the organs, is made taking into account the whole complex of changes noted at the autopsy.

In differential diagnosis, it should be borne in mind that the intestinal form of diplococcal infection has a great similarity in the pathoanatomical picture with colibacillosis, and the pulmonary form with paratyphoid. In such cases, the results of bacteriological examination are decisive for the diagnosis.

The final diagnosis of colisepticemia can always be made, taking into account the clinic of the disease, epizootological examination data, autopsy, bacterioscopic and bacteriological studies. In addition, in doubtful cases, they resort to infecting white mice with cultures isolated from the corpses of dead animals.

Bibliography

q Vertinsky K.N. "Pathological anatomy of farm animals" M. "Kolos" 1973

q Konapatkin A.A. "Episiootology and infectious diseases of farm animals" M. "Kolos" 191993

q M. "Keril and Methodius" 1997

Great Soviet Encyclopedia

Great Soviet Encyclopedia

pathological anatomy, pathological morphology, the science of the development of structural changes in a diseased organism. In a narrow sense, under pathological anatomy understand the study of macroscopic changes in the body, in contrast to pathological histology and pathological cytology, which reveal pathological processes using microscopy and histochemical examination. as an academic discipline pathological anatomy subdivided into general pathology, which studies the types of pathological processes regardless of the etiology of the disease, the type of animal, and the affected organ (necrosis, dystrophy, inflammation, etc.), organopathology, which studies the same processes depending on their localization, and special pathology, which studies the complex changes in a given disease. Organopathology and special pathological anatomy sometimes combined into a private pathological anatomy. Sources of material for the study of pathological anatomy - autopsy, biopsy, organs of experimental animals. pathological anatomy is closely related to pathological physiology, together with which it constitutes the science of a diseased organism - pathology, which is the foundation for medical and veterinary sciences.

The emergence of pathological anatomy is associated with the development of anatomy and physiology. The founder of pathological anatomy is the Italian physician G. Morgagni (1682-1771), who associated diseases with anatomical changes in organs. In the middle of the XIX century. cellular pathology arose (R. Virchow), which determined painful changes at the level of cells and tissues. pathological anatomy animals began to develop rapidly from the 2nd half of the 19th century. Abroad, prominent scientists in the field of veterinary pathological anatomy: in Germany - T. Kitt, E. Joost, K. Nieberle; in Romania - V. Babesh; in Hungary - F. Gutira, I. Marek and others. The beginning of the development of veterinary pathological anatomy in Russia was laid by the works of I. I. Ravich, A. A. Raevsky, N. N. Mari. The largest Soviet veterinary pathologists are K. G. Bol, N. D. Ball and their numerous students - B. K. Bol, B. G. Ivanov, V. Z. Chernyak, etc.

pathological anatomy animals is developing as a science, one with the pathological human anatomy. The work of Soviet pathologists studied morphological changes and their development in most diseases of agricultural, domestic animals, commercial mammals, birds and fish, which is important for understanding the essence of diseases, their diagnosis and testing the effectiveness of therapeutic measures. Veterinary pathologists pay special attention to the study of the pathomorphogenesis of infectious animal diseases, in particular viral, malignant tumors, and metabolic diseases; the dynamics of reparative processes, taking into account the physiological status of animals; embryonic pathology in various animal species; morphology of general pathological processes at the molecular and submolecular levels, etc.

Proteins play a major role in life processes. They are divided into simple and complex. The most important simple proteins are proteins: albumins and globulins; complex proteins - proteids: nucleoproteins, glucoproteins, chromoproteins, etc. The chemistry of protein metabolism in tissues in normal and pathological conditions has not yet been studied enough, therefore there is no rational classification of protein dystrophy.

The essence of protein dystrophies is that the structure of the cytoplasm of cells and intercellular substance is disturbed as a result of physicochemical changes in proteins, due to the redistribution of the amount of water in the tissues, the entry of protein substances foreign to the body brought by the blood into the tissues, an increase in cellular secretion, etc.

Depending on the predominant localization of morphological changes, dysproteinosis is usually divided into cellular, extracellular and mixed. By distribution, they can be general and local.

Cellular dysproteinoses include granular, hyaline-droplet, hydropic and horny dystrophy; to extracellular - hyalinosis and amyloidosis; to mixed - a violation of the exchange of nucleoproteins and glucoproteins.

Cellular dysproteinoses . Granular dystrophy- the appearance in the cytoplasm of grains and drops of a protein nature. The most common of all types of protein dystrophies. Parenchymal organs (kidneys, liver, myocardium) are involved in the dystrophic process, less often skeletal muscles. In this regard, granular degeneration is called parenchymal dystrophy.

Under the microscope, swelling of the epithelial cells of the kidneys, liver and muscle fibers is noted, as well as the formation of granularity in their cytoplasm, which causes a cloudy appearance of the cells.

The appearance of granularity may be associated with swelling and rounding of mitochondria under conditions of tissue hypoxia or is the result of decomposition of protein-lipoid complexes of the cytoplasm, pathological transformation of carbohydrates and fats into proteins, denaturation of cellular protein, or infiltration of cells with proteins foreign to the body brought with blood flow.

Macroscopically, organs with granular dystrophy are swollen, flabby in consistency. They are painted paler than normal, due to squeezing of the capillaries by swollen cells. When cut, the parenchyma swells, dull appearance, the pattern is smoothed. The heart muscle resembles meat scalded with boiling water, and the liver and kidneys are gray-brown in color.

The cause of granular dystrophy can be infectious diseases, various intoxications of the body, circulatory disorders and other factors leading to the accumulation of acidic products in the tissues.

Clinical significance: granular dystrophy can cause dysfunction of the affected organs, especially important ones such as the heart - the contractility of the myocardium is weakened.

Hyaline drop dystorphia- the appearance in the cytoplasm of large translucent homogeneous protein drops. This process is based on the resorption of pathological protein substances (paraproteins) by the cells when they appear in the plasma, or hyaline-like drops are formed due to the denaturation of their own cellular proteins. This dystrophy is noted in foci of chronic inflammation of tissues, glandular tumors, but especially often in the epithelium of the renal tubules with nephrosis and nephritis. During life, in animals with nephritis, protein and casts are found in the urine.

The outcome of hyaline-drop dystorphy is unfavorable, since this process turns into necrosis.

Vacuolar dystrophy is determined only under a microscope. Vacuolization of the cytoplasm, which is not related to hydropic dystrophy, is observed in the ganglia of the central and peripheral nervous system, as a manifestation of physiological secretory activity. Signs of vacuolization can be detected postmortem in tissues and organs containing large amounts of shcolene (liver, muscle tissue, nerve cells). This is due to the fact that in the corpse, under the action of enzymatic processes, glycolen is broken down, as a result of which vacuoles are formed in the cytoplasm. In addition to vacuolization of the cytoplasm, signs of cloudy swelling are also characteristic.

Vacuolar degeneration should not be confused with fatty degeneration, since in the process of manufacturing histological preparations using solvents (alcohol, xylene, chloroform), fatty substances are removed and vacuoles appear in their place. To differentiate these dystrophies, it is necessary to prepare sections on a freezing microtome and stain them for fat.

The outcome of hydropic dystophia is in most cases unfavorable, since cells die during this process.

Horny dystrophy(pathological keratinization) - the formation of a horny substance (keratin) in the cells. Normally, keratinization processes are observed in the epidermis. Under pathological conditions, it may have excessive horn formation (hyperkeratosis) and a qualitative violation of horn formation (parakeratosis). Cornification occurs in the mucous membranes (leukoplakia).

Examples hyperkeratosis are dry corns that develop from prolonged skin irritation. Under the microscope, a thickening of the epidermis is noted due to excessive layering of the horny substance and hyperplasia of the cells of the Malpighian layer. The horny substance is stained pink with eosin, and yellow with Van Gieson's picrofuchin mixture. Occasionally, horses with inflammatory skin diseases develop a spiky thickening of the epidermis due to hypertrophy of the spiky cell layer and elongation of the interpapillary epithelial processes. Such lesions are called acanthosis(Greek akantha - thorn, needle). Hyperkeratosis is referred to as ichthyosis(Greek ichtys - fish), which is a deformity. The skin of newborns in these cases is rough, hard due to the appearance of gray horny formations on it, like fish scales. Animals with such skin lesions usually die in the first days of life.

Excess horn formation is seen in warts, cancroid (a cancer-like tumor), and dermoid cysts.

Parakeratosis(Greek para - about, keratis - horny substance) - a violation of horn formation, expressed in the loss of the ability of epidermal cells to produce keratohyalin. In this condition, the stratum corneum is thickened, loose, and scales form on the surface of the skin. Under the microscope, discomplexed horny cells with rod-shaped nuclei are noted. Parakeratosis is observed in dermatitis and lichen lichen.

Leukoplakia- pathological keratinization of the mucous membranes, arising from the action of various irritants, with inflammatory processes and beriberi A. It occurs, for example, in pigs on the mucous membrane of the prepuce from chronic irritation with urine. On the mucosa, whitish-gray raised areas of various sizes are formed, rounded in shape, consisting of keratinized epithelium. Sometimes this phenomenon is observed in the urethra, bladder and rumen of ruminants. With avitaminosis A, the glandular epithelium of the oral cavity, pharynx and esophagus becomes keratinized.

In morphological and pathogenetic terms, pathological keratinization is essentially not associated with a violation of protein metabolism, but is closer to the process of hypertrophic tissue growth and metaplasia.

Encephalitis(Encephalitis)- inflammation of the brain. Inflammatory processes in the brain must be distinguished from dystrophic changes in nerve cells and fibers (pseudoencephalitis or encephalomalacia) with the subsequent development of reactive processes that are observed in metabolic disorders and intoxications.

Classification of encephalitis. By origin distinguish between primary encephalitis (rabies, Borna's disease and others caused by neurotropic viruses) and secondary as a complication of the underlying disease (swine, dog and bird plague, malignant catarrhal fever, myt, etc.) localization of the pathological process encephalitis is divided into:

1) polioencephalitis (polios - gray) - inflammation, observed mainly in the gray matter of the cortex or brain stem (it is typical for rabies, Bornais disease, enzootic encephalitis of sheep and cattle, epidemic human encephalitis and some others);

2) leukoencephalitis - changes occur mainly in the form of demyelination of nerve fibers and growth of neuroglia in the white matter of the brain;

3) panencephalitis - simultaneous position of both white and gray matter of the brain (register it with swine, dog and bird plague, malignant catarrhal fever, carnivorous encephalitis, infectious encephalomyelitis of horses, etc.);

4) meningoencephalitis - the inflammatory process spreads from the meninges to the brain and spinal cord.

By prevalence of the inflammatory process encephalitis is focal, disseminated and diffuse.

AT depending on a different combination of components of the inflammatory response observe: acute non-purulent encephalitis of the lymphocytic type, serous encephalitis, purulent and hemorrhagic. By downstream encephalitis can be acute, subacute and chronic.

The development of one form or another of encephalitis depends on the cause that causes it, the duration and strength of the pathogenic stimulus, and the reactive state of the organism itself. The clinical manifestation of encephalitis in its symptoms is diverse and depends on the localization and nature of the inflammatory process: increased irritability, attacks of violence, aggressiveness, depression, impaired motor functions, etc. Similar symptoms can also occur with inflammation of the meninges, which is important to take into account in pathomorphological studies.

Macroscopically non-purulent encephalitis is not always recognizable, since the signs of an inflammatory reaction in the brain substance are not bright. In the most pronounced cases, with encephalitis, flabbiness of the medulla, uneven redness, some smoothness of the cerebral gyri of the cerebral hemispheres, as well as hemorrhages, hypermia and swelling of the meninges, an increase in the amount of fluid in the lateral ventricles, which sometimes becomes reddish, are noted.

Microscopically alternative, exudative and proliferative processes are established in the brain tissue. Of change vascular connective tissue apparatus the most significant is the presence of vascular and perivascular cellular infiltrates of hematogenous and local origin (multiplication of endothelial and adventitial cells of small vessels, veins, pre- and capillaries). As a result, cellular muffs are formed around the vessels, consisting mainly of small lymphoid cells, single rounded histiocytes, monocytes, and even less often plasma cells. Transitional cell forms occur between lymphoid cells and histiocytes, which indicates the genetic relationship of the cell proliferate. In some places, cellular infiltrates extend beyond the perivascular spaces and are distributed in the surrounding glial tissue of the brain.

Of other changes in the vascular network, plethora, lumen expansion, regional stasis, thrombosis, swelling, proliferation, desquamation of the endothelium, sometimes segmental necrosis and hyalnosis of the vascular walls, perivascular edema and hemorrhages should be noted. Sometimes in the cells of the infiltrate, karyopyknosis and karyorrhexis are noted.

Glia changes are expressed by the multiplication of its cells and the appearance of degenerative forms among them (rod-shaped and fragmentation of the nuclei, barking). Proliferative processes on the part of glia are either focal or diffuse. At the same time, the polymorphism of its cells is noted, their transformation into wandering (mobile) forms. Glia proliferates are formed either around vessels or around nerve cells, and sometimes, independently of them, focal accumulations in the form of glial nodules are created. If the reproduction of glial cells takes place around nerve cells, then they speak of neuronophagy. Distinguish between true and false neuronophagy. True neuronophagy is considered to be one where the multiplication of glial cells occurs around the damaged nerve cell and only the cell glial nodule remains in place of the latter. False neuronophagy refers to the reproduction of the same elements of neuroglia around an intact nerve cell. In the chronic course of the disease (for example, with distemper), scars (gliosis, neuroglial sclerosis) can form from glial tissue.

Nerve cell changes in encephalitis are diverse and are in close connection with the nature and severity of the course of the process. The most important changes concern the chromatophilic, tigroid substance of the cytoplasm (Nissel grains). The process begins with swelling of the cytoplasm, combined with fine-grained, dusty disintegration of the Nissel grains up to their complete disappearance from the cell body (chromatolysis or tigrolysis). The essence of this process lies in the development of intracellular edema, which in the initial phases manifests itself in the form of partial chromatolysis either in the center of the nerve cell (perinuclear edema) or on the periphery (pericellular edema). Vacuoles often form in the marginal zone. Expressed forms of intracellular edema give the cytoplasm of the nerve cell the appearance of honeycombs. Electron microscopically note the disintegration of polysomes and ribosomes, vesiculation and expansion of the cistern of the endoplasmic reticulum, swelling and clearing of the mitochondrial matrix. The nuclei of nerve cells also undergo swelling, edema, and lysis. In the later stages, this process ends with complete lysis of the nerve cell (karyocytolysis).

In addition, changes in nerve cells are observed in the form of homogenization of the cytoplasm and nucleus, since the Nissel grains at the same time seem to merge into a homogeneous dark-colored mass (pyknosis or wrinkling of the nerve cell). The highest degree of such a process is defined as sclerosis of the nerve cell.

Neurofibrils can persist for a long time, but in most cases, along with changes in the chromatophilic substance, the neurofibrillary structure also changes. They form a finely looped network when sprayed with a tigroid substance or thicken unevenly, swell like varicose veins and break up into separate clumps and grains. Ultimately, they also undergo either hydrolytic melting (fibrillolysis) or fuse together and are more intensively impregnated with silver. In dystrophically altered nerve cells, myelin figures, drops of fat can be detected, and the pigment lipofuscin can accumulate. With complete dissolution of the tigroid substance, the neurofibrillary structure of the nerve cell usually completely disappears, which is revealed by silver impregnation or electron microscopy.

Along with the cytoplasm of nerve cells, changes in their nuclei are also noted: displacement of the nucleus to the periphery of the body of the nerve cell, swelling or wrinkling of it, change in shape (the nucleus acquires uneven contours), karyorrhexis, vacuolization and karyolysis. Sometimes the nucleolus shrinks, and it becomes like a mulberry. Nerve processes are also subject to dystrophic changes. They break down with the formation of detritus from myelin figures and fat droplets. In places of decay, mobile neuroglial cells appear, phagocytizing decay products and acquiring the appearance of granular balls. At the same time, along the course of the nerve processes, Schwann cells are usually activated, which are rounded, multiply with the formation of cell clusters. Then, in the intercellular substance of the nervous tissue, lytic processes begin to predominate, followed by softening of the brain, which is largely facilitated by serous exudation.

Dystrophic changes in nerve cells may be accompanied by structural changes that are compensatory and adaptive in nature, especially with a long course of the disease. These include hypertrophy of the nucleolus, nucleus and cells in general with hyperplasia of intracellular organelles, the appearance of binuclear cells, etc.

In many viral encephalitis, a specific process in nerve cells is the detection of inclusion bodies. These are acidophilic oval or round bodies with a certain internal structure. In some diseases, they are formed in the cytoplasm (rabies, plague, etc.), and in others, in the nuclei (enzootic encephalitis of horses, sheep, etc.). Inclusion bodies are formed as a product of the interaction of elementary bodies of the virus with nucleic acids and plasma proteins. Their nature and significance for the organism have not yet been studied enough, but they are of great diagnostic value.

Other forms of encephalitis (serous, hemorrhagic) are relatively rare in animals. Serous encephalitis of an infectious, toxic or allergic nature is manifested by swelling of the brain tissue. Hemorrhagic encephalitis is characterized, along with the changes mentioned above, by diapedesis of erythrocytes and their increased admixture to the inflammatory exudate. It is sometimes recorded in diseases caused by neurotropic viruses (Born's disease, etc.), swine fever, feed poisoning, botulism, etc. Macroscopically, individual or multiple foci of softening of a dark red or red-brown color are found, which differ from hemorrhages in that the hemorrhagic exudate does not coagulate. Histologically, they show strongly injected vessels, hemorrhagic exudate in the perivascular lymphatic spaces. Ganglion cells undergo necrobiosis and necrosis. Hemorrhagic encephalitis causes death very quickly.

Diplococcal septicemia is a predominantly acute infectious disease of young animals, affecting more often calves and lambs, less often foals and piglets. Clinical and anatomically characterized by a picture of acute sepsis. The causative agent of the disease is diplococcus.

Pathogenesis- Under natural conditions, infection occurs through the respiratory tract and the gastrointestinal tract. In places of primary introduction, diplococci multiply and subsequently penetrate into the lymphatic and blood tracts. With blood and lymph, the pathogen spreads through organs and tissues. Pathogen strains have toxinogenic properties, they secrete toxic products that suppress phagocytosis and increase the permeability of the vascular walls, which contributes to the hemolysis of red blood cells, the blood coagulation process is disturbed - toxemia develops with symptoms of hemorrhagic diathesis and severe organ damage.

Pathological changes. At hyperacute current infections at the autopsy of dead animals find multiple point and small-spotted hemorrhages on the mucous membrane of the small intestine, less often on the abomasum, on the mesentery, peritoneum, under the epicardium and endocardium. Acute hyperemia of the mucous membranes of the nasal cavity, larynx, trachea, severe hyperemia and serous pulmonary edema are also noted.

At acute course Depending on the routes of infection and the penetration of the pathogen into the body of the animal, the respiratory or digestive apparatus is predominantly affected.

When the respiratory apparatus is affected, conjunctival hyperemia, catarrhal inflammation of the mucous membrane of the upper respiratory tract, swelling and enlargement of bronchial lymph nodes, effusion into the chest cavity of serous or serous-hemorrhagic exudate, multiple petechial hemorrhages and fibrin deposits on the pleura, pericardium, serous-hemorrhagic or croupous pneumonia are noted. with a predominant lesion of the anterior and middle lobes, less often with coverage of the entire lung tissue; hemorrhages under the epi- and endocardium; dystrophic changes in the liver, kidneys and myocardium, enlargement of the spleen.

In cases where the infection occurs with a lesion of the gastrointestinal tract, hemorrhagic effusion is found in the abdominal cavity in large numbers; the spleen is sharply enlarged (2-3 times), rubber-like (rubber) consistency, with rounded edges, dotted and striped hemorrhages under the capsule. The liver is swollen, plethoric. Under the capsule of the kidneys, multiple small hemorrhages. More striking changes in the gastrointestinal tract; the mucous membrane of the abomasum and the small intestine is sharply hyperemic, in a state of serous edema, dotted with dotted and small-spotted hemorrhages; liquid contents in the intestinal cavity, in some cases painted red

(due to the admixture of blood). Similar signs, but weaker, are noted in the large intestine, especially in the blind and colon.

Mesenteric lymph nodes are strongly swollen, enlarged, gray-red in color, numerous petechial hemorrhages can be seen on the cut surface. Sometimes in the acute course of the disease, the respiratory organs and the gastrointestinal tract are simultaneously affected.

Diplococcal infection also occurs in adult animals (in cows, mares, sows and ewes), which are most often the source of infection for young animals (in utero, through milk, urine, nasal discharge). Pathological and anatomical changes in them are usually expressed in the development of catarrhal, catarrhal-purulent endometritis and mastitis.

The diagnosis of diplococcal septicemia in young animals, due to the absence of specific processes in the organs, is made taking into account the whole complex of changes noted at the autopsy.

In differential diagnosis, it should be borne in mind that the intestinal form of diplococcal infection has a great similarity in the pathoanatomical picture with colibacillosis, and the pulmonary form with paratyphoid. In such cases, the results of bacteriological examination are decisive for the diagnosis.

The final diagnosis of colisepticemia can always be made, taking into account the clinic of the disease, epizootological examination data, autopsy, bacterioscopic and bacteriological studies. In addition, in doubtful cases, they resort to infecting white mice with cultures isolated from the corpses of dead animals.

Bibliography

q Vertinsky K.N. "Pathological anatomy of farm animals" M. \\ "Kolos" \\ 1973

q Konapatkin A.A. "Episiootology and infectious diseases of farm animals" M. \\ "Kolos" \\ 191993

q Great Soviet Encyclopedia M.\\ "Keril and Methodius" \\ 1997

Great Soviet Encyclopedia

Great Soviet Encyclopedia

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Hosted at http://www.allbest.ru/

• 7. Mechenchymal and epithelial tumors
• 8. Protocol of diagnostic and act of forensic veterinary autopsy
• 9. Judicial deontology (violations of professional activity in the field of veterinary medicine)
• List of used literature

1. Violation of glycoprotein metabolism

Glycoproteins- complex compounds of protein with polysaccharides containing hexoses, hexosamines and hexuronic acids. These include mucins and mucoids.

Mucins form the basis of the mucus secreted by the epithelium of the mucous membranes and glands. Mucus has the appearance of a translucent viscous substance that falls out under the influence of weak acetic acid or alcohol in the form of a thin fibrous mesh. The composition of the mucus includes neutral or acidic polysaccharides - protein complexes containing hyaluronic and chondroitin sulfuric acids (glycosaminoglycans), which give the mucus chromotropic or metachromatic properties. Thionin and cresyl violet turn mucus red and tissues blue or purple. Mucicarmine gives it a red color, and toluidine blue - lilac - pink. Mucin protects mucous membranes from physical damage and irritation from chemicals.

Mucus formation as a pathological process has a protective and adaptive value. Mucin protects mucous membranes from physical damage and irritation from chemicals. Mucus is the carrier of digestive enzymes.

Mucoids, or mucus-like substances ("pseudomucins"), are not homogeneous chemical compounds containing protein and glycosaminoglycans. They are part of various tissues: bones, cartilage, tendons, heart valves, arterial walls, etc. In embryonic tissues, mucoids are contained in large quantities, including in the umbilical cord of newborns. They have common physico-chemical properties with mucus. Mucoids are alkaline and, unlike mucin, are not precipitated by alcohol or acetic acid.

morbid anatomy farm animal

Mucosal degeneration is accompanied by the accumulation of mucus and mucus-like substances in the tissues. There are two types of it: cellular (parenchymal) and extracellular (mesenchymal).

Cellular (parenchymal) mucousdystrophy- violations of the metabolism of glycoproteins in the glandular epithelium of the mucous membranes, which are manifested by hypersecretion of mucus, a change in its qualitative composition and the death of secreting cells.

Mucosal degeneration often occurs with catarrhal inflammatory processes on the mucous membranes as a result of direct or indirect (reflex) action of various pathogenic stimuli. It is noted for diseases of the digestive, respiratory and genitourinary organs.

Irritation of the mucous membranes causes an expansion of the secretion area and an increase in the intensity of mucus formation, as well as a change in the physicochemical properties of the composition of the mucus itself.

Histologically mucosal degeneration is characterized by hypersecretion or excessive formation of mucin in the cytoplasm of epithelial cells lining the mucous membranes, increased mucus secretion, death and desquamation of secreting cells. Mucus can close the excretory ducts of the glands and cause the formation of retention cysts, which is facilitated by squeezing them with growing connective tissue. With a rarer polypous catarrh, on the contrary, hyperplasia is observed not only of the glandular, but also of the connective tissue.

Macroscopically the mucous membrane is swollen, dull, covered with a thick layer of mucus, in acute inflammation of the organ it is hyperemic with hemorrhages, and in chronic inflammation it is compacted due to the growth of connective tissue. The mucus produced in large quantities, depending on the degree of hydration or dehydration and the number of desquamated cells, is of different consistency and viscosity. Depending on the type of inflammation of the organ, exudate of various properties (serous, purulent, hemorrhagic) is mixed with mucus.

functional meaning and Exodus mucosal degeneration depend on the intensity and duration of the process. With the elimination of pathogenic factors, regeneration of the epithelium due to cambial cellular elements can lead to a complete restoration of the affected organs. A long-term dystrophic process is accompanied by the death of the cellular elements of the epithelium, the growth of connective tissue and atrophy of the glands. In other cases, a pronounced functional insufficiency of the organ is noted (for example, partial loss of the digestive function of the organs of the gastrointestinal tract and in chronic catarrh with the development of exhaustion, etc.).

A peculiar kind of glycoprotein metabolism disorder is colloidal distrofia ( from the Greek colla - glue), which is characterized by excessive formation and accumulation of a colloidal mass of pseudomucin in the glandular organs (thyroid glands, kidneys, adrenal glands, pituitary gland, ovaries, mucous membranes), as well as in cystoadenomas. This dystrophy occurs with colloid goiter associated with iodine deficiency (an endemic disease of humans and animals in certain geobiochemical zones)

Macroscopically hypersecretion of the colloid, its accumulation in the follicles, atrophy of the glandular tissue, rupture of the membranes and fusion of the follicles with the formation of cysts are observed. Newly formed glandular follicles by budding from the previous ones can also undergo colloidal degeneration.

Macroscopically the thyroid gland, less often other glandular organs increase in volume, become uneven from the surface, cysts with viscous glue-like contents from grayish-yellow to dark brown are found on the cut .

Colloidal dystrophy causes functional failure of the organ. With colloid goiter, a general mucous edema of the connective tissue (myxedema) develops.

Extracellular (mesenchymal) mucousdystrophy ( mucus, mucous metamorphosis) is a pathological process associated with the accumulation of chromotropic substances in connective hiccups (fibrous, fatty, cartilaginous and bone).

Causes tissue dystrophy: exhaustion and cachexia of any etiology, such as starvation, chronic diseases (tuberculosis, malignant tumors, etc.) and dysfunction of the endocrine glands (colloidal goiter, etc.). The essence of mucous metamorphosis consists in the release of a chromotropic substance (glycosaminoglycans) from the connection with the protein and its accumulation in the main substance of the connective tissue.

Histologically in contrast to mucoid swelling, collagen fibers are dissolved and replaced by a mucus-like mass. At the same time, cellular elements become isolated, swell, acquire an irregular shape: multi-processed or stellate, and also dissolve.

Macroscopically the affected tissues become swollen, flabby, gelatinous, impregnated with a semi-translucent mucus-like mass.

functional meaning and Exodus of this process are determined by the degree and place of its development. In the initial stages of mucus, the elimination of the cause is accompanied by the restoration of the structure, appearance and function of the affected tissue. As the process develops, complete liquefaction and colliquation necrosis of the tissue occur with the formation of cavities filled with a mucus-like mass.

2. Formation of stones and calculi

Calculi are dense or solid formations that lie freely in the natural cavities of organs and excretory ducts of glands. They arise from the organic matter of protein origin and salts of various composition, which fall out of the secrets and excretions of the abdominal organs.

The composition, size, shape, consistency and color of stones depend on the conditions and place of their formation. In farm animals, calculi are most often found in the gastrointestinal tract, kidneys, urinary tract, gallbladder and bile ducts, pancreas and salivary glands, less often in other organs.

Gastrointestinal stones are divided into true, false, phytobezoars, pylobezoars, conglobats and plumestones.

True stones, or enteroliths, consist mainly (90%) of ammonia-magnesium phosphate, calcium phosphate and other salts. They have a spherical or irregular shape, a hard consistency and resemble a cobblestone. Their surface is rough, smooth, sometimes polished (faceted) as a result of a tight fit of stones. The color of freshly extracted stones is dark brown, and after the surface layer has dried, it is grayish white. A characteristic feature of enteroliths is the layered structure of the cut surface, on the fault - radial radiance, which indicates the staging of their growth. In the center of the stone there may be a foreign body (a piece of metal, brick, felt, bone, etc.), which served as the main crystallization. These stones vary from a pea to 20-30 cm in diameter, weight - up to 11 kg. Small stones are found up to tens and hundreds, large ones are usually single.

False stones, or pseudoenterolitis, have a rounded shape, consist mainly of organic substances, but also contain mineral salts in small quantities. More often they are found in the colon of horses, as well as in the proventriculus and intestines of ruminants. Formed when eating food mixed with earth and sand. Their surface resembles them like a shelled walnut, diameter from 1-2 to 20 cm or more, weight up to 1 kg (sometimes more), quantity - from one to several tens.

Phytocalculi ( from lat. Phyton - plant) are formed from plant fibers. They are light, spherical in shape, their surface is smooth or rough-hilly, the consistency is loose. Break easily. More common in ruminants in the proventriculus.

Sawstones(from Latin Pilus - hair), or hairballs, bezoars, are found in the stomach and intestines of cattle and small cattle. Animals, especially young animals, with a lack of salt in the diet and a violation of mineral metabolism, lick their coat and each other (lizukha), swallow wool, which is enveloped in mucus and falls off with the formation of balls. The author observed 25 or more wool balls in the stomach and intestines of lambs under mineral starvation, as a result of which they licked and swallowed the wool of their mothers. The lambs died from starvation.

conglobates- calculi from undigested food particles and stuck together feces with an admixture of foreign bodies (rag, earth, etc.). most common in horses in the large intestine with atony. Dogs and cats sometimes have formations of feathers.

Urinary stones found in cattle, horses, fur-bearing animals (mink, etc.), including at a young age. Their formation in the renal tubules, pelvis and bladder is associated with urolithiasis, which occurs when excessive feeding of mineral salts, a general violation of mineral and protein metabolism, as well as a lack of vitamins, especially A. In birds, their appearance in the kidneys is associated with gout due to metabolic disorders nucleoproteins. The structure, shape, size and color of the stones depend on the chemical composition and type of animal. They consist of uric acid, urates, oxalates, carbonates, phosphates, cystine xanthine. Therefore, according to the composition, urate, phosphate, oxalate, calcareous and mixed stones are distinguished. Quite often stones have an appearance of the casts repeating the form of cavities (a renal pelvis). There are single and multiple stones. The surface of the stones is usually smooth, granular or spiny, the cut pattern may be layered.

Salts can also fall out in the form of sand (urosedimenta).

Biliary stones found in the gallbladder and bile ducts of cattle and pigs cholelithiasis disease. They are single and multiple. Their size varies from a few millimeters to 10 cm or more. In pigs after fattening, a stone with a goose egg was found. The shape of the stones copies the cavity in which they are formed. Their composition: organic protein base, calcium salts, bile pigments and cholesterol. Depending on the composition, calcareous, pigmented and mixed stones are distinguished. Cholesterol stones are almost never found.

Salivary stones (sialoliths) more often noted in horses in the excretory duct of the salivary gland. In ruminants, it is found in the pancreatic duct. A foreign body is sometimes found in the center of them: oat grain, straw, etc. The mineral basis is calcium salts. Therefore, they are usually white and dense. Their size and number vary.

functionalmeaningandExodus stone formations are different. Many stones are of no clinical significance and are found only incidentally during sectioning. However, the formation of stones, especially enteroliths, can have significant consequences. The stones cause tissue atrophy, inflammation of the abdominal organs, necrosis of the walls of the cavities, their perforation with the formation of penetrating ulcers, fistulas, and blockage of the excretory ducts, which prevents the contents from moving. In the latter case, due to irritation of the nerve receptors, spastic contractions of the ducts with pain attacks (colic) are noted. Due to the pressure of the stone on the tissue during blockage of the intestine, the wall of the latter dies and, on this basis, intoxication of the body develops with a fatal outcome.

3. Violation of the content of tissue fluid

In animals, the tissues of the internal environment of the body include three types of fluid: blood, lymph and tissue fluid. Their content is closely interconnected and regulated by a complex neurohumoral mechanism. With an increase in the amount of tissue fluid, edema, dropsy, hydrops (from the Greek. Hydrops - dropsy), edema (from the Latin. Exicosis - dry), dehydration occur.

Tissue fluid is poor in protein (up to 1%) and is normally associated with protein colloids: collagen and interstitial substance. An increase in the amount of tissue fluid, i.e. the development of edema or dropsy occurs due to increased permeability of the capillary walls and resorption insufficiency of the lymphatic system. The edematous fluid is not bound by protein colloids and freely flows out when the tissue is cut. It is transparent and contains 1-2% protein, a small amount of cells and is called a transudate (from Latin trans-through).

The accumulation of edematous fluid in the subcutaneous tissue - anasarca (from the Greek. Ana - over and sarcos - meat), in the cavity of the heart shirt - hydropericarditis, in the pleural cavity - hydrothorax, in the abdominal cavity - ascites (from the Greek. Ascites - bag), in the cavity the vaginal membrane of the testes - hydrocele, in the ventricles of the brain - hydrocephalus. Causes, pathogenesis and types of edema are varied. However, the main reason is the retention of sodium and water by the body, a decrease in the osmotic pressure of the blood and the permeability of the capillaries of the membranes, stagnation in the movement of blood and lymph.

There are cardiac edema (sodium retention), congestive (mechanical), renal, dystrophic, inflammatory, allergic, toxic, angioedema, traumatic. A special type is swelling of pregnant women, which develop as a result of toxicosis or as a result of squeezing of the veins by an enlarged uterus.

Edema of the skin leads it to a strong thickening due to an increase in the layer of subcutaneous tissue (with inan in horses). Pulmonary edema often accompanies a number of diseases and is characterized by sleepy, doughy lungs, with a yellowish or bloody fluid flowing from the lumen of the bronchi. With cerebral edema, the convolutions are smoothed out, the amount of fluid in the subarachnoid space increases. In the heart shirt of horses and cattle there can be up to 5-10 liters of edematous fluid. In the abdominal cavity in large animals, it accumulates up to 50-100 liters, and with ascites in dogs - up to 20, in pigs - up to 30, in sheep - up to 40 liters.

Microscopically, edema is characterized by defibration and thickening of the connective tissue base of organs and expansion of cellular elements by edematous fluid. Serous transudate is usually poor in cellular composition and protein and stains light pink with hematoxylin-eosin.

Edema and dropsy are reversible processes: they disappear after the elimination of the causes that caused them. The transudate is absorbed and the damaged tissue is repaired. Only prolonged edema is irreversible, causing deep changes in the tissues.

The prevalence and outcome of edema largely depend on the causes that caused them. So, allergic edema easily passes after the elimination of the corresponding cause. Edema of the lungs and brain is very life-threatening. Dropsy of serous cavities impedes the activity of internal organs, in particular the heart, therefore, with it, they resort to pumping out transudate, for example, from the abdominal cavity with ascites. Transudate can serve as a good nutrient medium for microflora, and then inflammation easily occurs against this background.

Along with edema, tissue swelling should be distinguished - hydration. It can occur in the white matter of the brain and cause death.

The process opposite to edema is exsicosis, dehydration, dehydration - a condition in which the body loses water. Especially often exsicosis occurs in young animals in violation of feeding, dyspepsia and diarrhea of ​​various etiologies. The appearance of animals with exsicosis is quite characteristic: sunken wings of the nose, eyes, dry mirror, wrinkled flabby skin, severe emaciation. The blood in such animals thickens, becomes dark, the surfaces of the serous membranes are dry or covered with a mucus-like viscous mass. At autopsy, all internal organs are reduced in size (atrophy), their capsule is thickened, wrinkled. Such post-mortem changes are especially pronounced in newborn animals that died from toxic dyspepsia, anaerobic dysentery and colibacillosis.

4. Regeneration of tissues and organs

Blood,lymph,bodiesblood - andlymphatic creation have high plastic properties, are in a state of constant physiological regeneration, the mechanisms of which also underlie reparative regeneration arising from blood loss and damage to the organs of blood and lymphopoiesis. On the first day of blood loss, the liquid part of the blood and lymph is restored due to the absorption of tissue fluid into the vessels and the flow of water from the gastrointestinal tract. Platelets and leukocytes are restored within a few days, erythrocytes - a little longer (up to 2-2.5 weeks), later the hemoglobin content is leveled. Reparative regeneration of blood and lymph cells during blood loss occurs by enhancing the function of the red brain of the spongy substance of the vertebrae, sternum, ribs and tubular bones, as well as the spleen, lymph nodes and lymphoid follicles of the tonsils, intestines and other organs. Intramedullary (from Latin intra - inside, medulla - bone marrow) hematopoiesis ensures the entry of erythrocytes, granulocytes and platelets into the blood. In addition, during reparative regeneration, the volume of myeloid hematopoiesis also increases due to the transformation of fatty bone marrow into red bone marrow. Extramedullary myeloid hematopoiesis in the liver, spleen, lymph nodes, kidneys and other organs occurs with large or prolonged blood loss, malignant anemia of infectious, toxic or alimentary-metabolic origin. The bone marrow can be restored even with great destruction.

Pathological regeneration blood and lymph cells with a sharp inhibition or perversion of hemo- and lymphopoiesis is observed in severe lesions of the blood and lymphatic organs associated with radiation sickness, leukemia, congenital and acquired immunodeficiencies, infectious and hypoplastic anemia.

Spleenandlymph nodes when damaged, they are restored according to the type of regenerative hypertrophy.

Circulatoryandlymphaticcapillaries have high regenerative properties even with large damage. Their neoplasm occurs by budding or autogenously.

During the regeneration of microvessels through budding the endothelium of capillaries multiplies with the formation of cell clusters or strands. From the kidney-shaped outgrowths, tubules lined with endothelium are formed, into the lumen of which blood or lymph enters from the preexisting capillary, blood or lymph flow is restored. All components of the vascular wall are formed from the perithelium and young connective tissue cells. They regenerate and grow into the vascular wall of the nerve endings.

At autogenous neoplasm of capillaries in the connective tissue surrounding the vessels, clusters of undifferentiated connective tissue cells appear, in the gap between which blood and lymph enter from preexisting capillaries, followed by the formation of the endothelial layer and other layers of the capillary wall. In the future, capillaries, with appropriate functional activity, can be rebuilt into vessels of the arterial or venous type. In this case, the smooth muscle cells of the vascular walls are formed as a result of metaplasia of undifferentiated connective tissue cells. The large arterial and venous vessels themselves have incomplete regeneration. When they are damaged (trauma, arteritis, phlebitis, aneurysm, varix, atherosclerosis), the intima (endothelial layer) is partially restored, other layers of the vessel wall are replaced by connective tissue. The resulting scar tissue causes narrowing or obliteration of the vessel lumen.

Physiological regeneration fibrousconnectivefabrics occurs by reproduction of lymphocyte-like mesenchymal cells originating from a common stem cell, poorly differentiated young fibroblasts (from Latin fibro-fiber, blastano-forming), as well as myofibroblasts, mast cells (labrocytes), pericytes and endothelial cells of microvessels. Mature, actively synthesizing collagen and elastin fibroblasts (collagen- and elastoblasts) differentiate from young cells. Fibroblasts first synthesize the basic substance of the connective tissue (glycosaminoglycans), tropocollagen and proelastin, and then tender reticular (argyrophilic), collagen and elastic fibers are formed from them in the intercellular space.

Reparative regeneration connective tissue occurs not only when it is damaged, but also with incomplete regeneration of other tissues, with wound healing. At the same time, a young juicy tissue is first formed with a large number of poorly differentiated young fibroblasts, as well as leukocytes, plasmablasts and labrocytes, which surround the newly formed thin-walled capillaries in a muff-like manner. Between fibroblasts with light (silvering method) and electron microscopy, the thinnest argyrophilic reticular fibers located in the ground substance are detected. The loops of such vessels protruding above the surface of the wound give it a bright red granular appearance, therefore the tissue is called granulation tissue (from Latin granules - grain). As the cellular elements of the vessels differentiate into arteries and veins and the formation of collagen fibers, the transformation of granulation tissue into mature fibrous tissue. Subsequently, the fibroblasts of the long-lived population flatten and transform into differentiated fibrocides, while the fibroblasts of the short-lived population die after they have performed their genetically programmed function. Ultimately, the fibrous tissue turns into a cavitary coarse fibrous scar tissue.

Pathological regeneration fibrous connective fabrics , associated with its complication by chronic irritation, a long-term inflammatory process or plastic insufficiency, is manifested by a delay in differentiation and maturation, or with an increased synthetic function of fibroblasts, excessive formation of fibrous and scar tissue with an outcome in hyalinosis. With such pathological regeneration of the wound, especially after burns and other severe injuries, keloid scars are formed (from the Greek kelё - swelling, swelling and eides-view) - tumor-like growths of scarred connective tissue of the skin at the site of the burn, protruding above the surface of the skin. Neoplasm and overgrowth of connective tissue are observed in proliferative inflammation (cirrhosis and in infectious granulomas), as well as in organization (encapsulation) and around foreign bodies.

Regenerationbonefabrics occurs as a result of the multiplication of osteogenic cells - osteoblasts in the periosteum and endosteum. Reparative regeneration in case of a bone fracture, it is determined by the nature of the fracture, the state of bone fragments, periosteum and blood circulation in the area of ​​damage. Distinguish between primary and secondary bone fusion.

Primary bone fusion observed with immobility of bone fragments and is characterized by ingrowth of osteoblasts, fibroblasts and capillaries into the area of ​​the defect and bruising. This is how a preliminary, or provisional, connective tissue callus is formed.

Secondary bone adhesions often observed in complex fractures, mobility of fragments and unfavorable conditions of regeneration (local circulatory disorders, extensive damage to the periosteum, etc.) In this type of reparative regeneration, the union of bone fragments occurs more slowly, through the stage of formation of cartilaginous tissue (preliminary bone and cartilaginous callus), which then undergoes ossification.

Pathological regeneration bone fabrics associated with general and local disorders of the regenerative process, prolonged circulatory disorders, death of bone fragments, inflammation and suppuration of wounds. Excessive and incorrect neoplasm of bone tissue leads to bone deformity, the appearance of bone outgrowths (osteophytes and exostoses), the predominant formation of fibrous and cartilaginous tissue due to insufficient differentiation of bone tissue. In such cases, with the mobility of bone fragments, the surrounding tissue takes the form of ligaments, a false joint is formed.

Regenerationcartilaginousfabrics occurs due to the chondroblasts of the perichondrium, which synthesize the main substance of the cartilage - chondrin and turn into mature cartilage cells - chondrocytes. Complete restoration of cartilage is observed with minor damage. Most often, incomplete restoration of cartilage tissue is manifested, its replacement with a connective tissue scar.

Regenerationfattyfabrics occurs due to cambial fat cells - lipoblasts and an increase in the volume of lipocytes with the accumulation of fat, as well as due to the reproduction of undifferentiated connective tissue cells and their transformation as lipids accumulate in the cytoplasm into the so-called cricoid cells - lipocytes. Fat cells form lobules surrounded by a connective tissue stroma with vessels and nerve elements.

Regeneration of muscle tissue is both physiological and after starvation, white muscle disease, myoglobinuria, toxicosis, bedsores, infectious diseases associated with the development of atrophic, dystrophic and necrotic processes.

Skeletal striated muscular the cloth has high regenerative properties during storage of the sarcolemma. The cambial cellular elements located under the sarcolemma - myoblasts - multiply and form a multinuclear symplast in which myofibrils are synthesized and striated muscle fibers are differentiated. If the integrity of the muscle fiber is violated, the newly formed multinuclear symplasts in the form of muscle buds grow towards each other and, under favorable conditions (a small defect, the absence of scar tissue), restore the integrity of the muscle fiber. However, in most cases, with major injuries and violation of the integrity of muscle fibers, the site of injury is filled with granulation tissue, a connective tissue scar is formed that connects the newly formed multinuclear flask-shaped bulges (muscle buds) of torn muscle fibers.

Cardiac striated muscular the cloth regenerates by the type of regenerative hypertrophy. In intact or dystrophically altered myocardiocytes, the structure and function are restored due to organelle hyperplasia and fiber hypertrophy. With direct necrosis, myocardial infarction and heart defects, incomplete restoration of muscle tissue can be observed with the formation of a connective tissue scar and with regenerative myocardial hypertrophy in the remaining parts of the heart.

Complete regeneration smooth muscular fabrics occurs by division of myoblasts and myofibroblasts. Muscle cells are able to grow into the site of damage and repair defects. Large damage to smooth muscles is replaced by scar tissue. In the remaining muscle, regenerative hypertrophy of muscle cells occurs.

Regenerationnervousfabrics. Ganglion cells of the brain and spinal cord during life are intensively renewed at the molecular and subcellular levels, but do not multiply. When they are destroyed, intracellular compensatory regeneration (organelle hyperplasia) of the remaining cells occurs. Compensatory-adaptive processes in the nervous tissue include the detection of multinucleolar, binuclear and hypertrophied nerve cells in various diseases accompanied by dystrophic processes, while maintaining the overall structure of the nervous tissue. The cellular form of regeneration is characteristic of neuroglia. Dead glial cells and small defects in the brain and spinal cord, autonomic ganglia are replaced by proliferating neuroglia and connective tissue cells with the formation of glial nodules and scars. Nerve cells of the autonomic nervous system are restored by hyperplasia of organelles, and the possibility of their reproduction is not excluded.

Peripheral nerves completely regenerate, provided that the connection of the central segment of the nerve fiber with the neuron is preserved and there is a slight divergence, the peripheral segment of the nerve fiber, its axial cylinder and the myelin sheath undergo disintegration; in the central segment, the death of these elements occurs only before the first intercepts of Ranvier. Lemmocytes form a myelin sheath and, finally, nerve endings are restored. Regenerative hyperplasia and hypertrophy of nerve terminals, or receptors, pericellular synaptic apparatuses and effects complete the structural and functional process of restoring innervation.

In violation of nerve regeneration (significant divergence of parts of the cut nerve, disorder of blood and lymph circulation, the presence of inflammatory exudate), a connective tissue scar is formed with disordered branching of the axial cylinders of the central segment of the nerve fiber in it. In the stump of the limb after its amputation, excessive growth of nerve and connective tissue elements can lead to the emergence of the so-called amputation neuroma.

Regenerationepithelialfabrics. The integumentary epithelium is one of the tissues with a high biological potential for self-healing. Physiological regeneration stratified squamous keratinizing epithelium of the skin occurs constantly due to the reproduction of cells of the germinal (cambial) malpighian layer. At reparative regeneration of the epidermis without damage to the basement membrane and the underlying stroma (abrasions, aphthae, erosion), increased reproduction of cells (keratinocytes) of the producing or basal layer is noted, their differentiation with the formation of germinal (basal and prickly), granular, shiny and horny layers associated with synthesis in their in the cytoplasm of a specific protein - keratohyalin, which turns into eleidin and keratin ( complete regeneration). When the epidermis and stroma of the skin are damaged, the cells of the germ layer along the edges of the wound multiply, crawl onto the restored membrane and stroma of the organ and cover the defect (wound healing under the scab and by primary intention). However, the newly formed epithelium loses the ability to completely differentiate the layers characteristic of the epidermis, covers the defect with a thinner layer and does not form skin derivatives: sebaceous and sweat glands, hairline ( incomplete regeneration). An example of such regeneration is wound healing by secondary intention with the formation of a dense white connective tissue scar.

integumentary epithelium mucous shells digestive, respiratory and genitourinary tracts (stratified flat non-keratinizing, transitional, single-layer prismatic and multinuclear ciliated) is restored by reproduction of young undifferentiated cells of the crypts and excretory ducts of the glands. As they grow and mature, they transform into specialized cells of the mucous membranes and their glands.

Incomplete regeneration of the esophagus, stomach, intestines, ducts of glands and other tubular and cavity organs with the formation of connective tissue scars can cause their narrowing (stenosis) and expansion, the appearance of unilateral protrusions (diverticula), adhesions (sinechia), incomplete or complete overgrowth (obliteration) of organs (cavities of the heart bag, pleural, peritoneal, articular cavities, synovial bags, etc.)

Regeneration of the liver, kidneys, lungs, pancreas, and other endocrine glands proceeds at the molecular, subcellular and cellular levels based on patterns inherent in physiological regeneration, with great intensity. Reparative regeneration of dystrophically altered parenchymal organs is characterized by a slowdown in the rate of regeneration, but when the action of a pathogenic stimulus is eliminated, under favorable conditions, the rate of regeneration is accelerated and complete restoration of the damaged organ is possible. With multiple liver biopsies of highly productive cows and after their slaughter, it was found that in the organ with metabolic pathology (ketosis, osteodystrophy and other diseases), along with destructive changes in hepatocytes from the very beginning of the disease, compensatory-adaptive, recovery processes, which indicates the body's ability to mobilize exogenous and reserve nutrients with the restoration of the structure and function of the organ. With focal irreversible damage (necrosis) in parenchymal organs, as well as with partial resection of them (from limited resection to removal of 3/4 of the liver, 4/5 of the thyroid gland and 9/10 of the adrenal cortex), the mass of the organ can be restored according to the type of regenerative hypertrophy. At the same time, in the preserved part of the organ, reproduction and an increase in the volume of cellular and tissue elements are observed, and scar tissue is formed at the site of the defect ( incomplete recovery).

Pathological regeneration of parenchymal organs is observed with various long-term, often recurring damage to them (circulatory and innervation disorders, exposure to toxic toxic substances, infections). It is characterized by atypical regeneration of epithelial and connective tissues, structural restructuring and deformation of the organ, the development of cirrhosis (cirrhosis of the liver, pancreas, nephrocyrrhosis, pneumocirrhosis).

5. Proliferation, regulation of inflammation, significance and outcome of inflammation

Proliferation (from lat. proles - descendant, fero - wear, create) - the final phase of inflammation with the restoration of damaged tissue or the formation of a scar. In this phase of inflammation, as a result of alternative and exudative processes, under the influence of biologically active substances, anabolic processes are stimulated, the synthesis of RNA and DNA in cells, specific enzymatic and structural proteins, histiogenic and hematogenous cells multiply: cambial, adventitial and endothelial cells, B - and T - lymphoblasts and monoblasts, plasma cells and labrocytes, fibroblasts, lymphocytes, histiocytes and macrophages, including mature macrophages, or epithelioid cells, are differentiated, and with incomplete fusion of the latter (the cytoplasm merges into a common mass with a large number of nuclei), the largest macrophages or giant cells (Langhans cells or foreign bodies). Proliferating fibroblasts synthesize the main substances of the connective tissue - tropocollagen (collagen precursor) and collagen, turn into mature cells - fibrocytes.

During inflammation in the process of proliferation, complete or incomplete regeneration of not only connective tissue, but also other damaged tissues occurs, atrophied and dead parenchymal cells, integumentary epithelium are replaced, new vessels are differentiated, nerve endings and nerve connections are restored, as well as cells that provide local hormonal and immune homeostasis.

The regulation of inflammation is carried out with the participation of mediator, hormonal, immune and nervous regulatory mechanisms. Cellular cyclic nucleotides play an important role in the regulation of mediation. Cyclic guanosine monophosphate (cGMP) in the presence of divalent cations (Ca ++, Mg ++) accelerates the release of mediators, and cyclic adenosine monophosphate (cAMP) and factors that stimulate the adenylate cyclase system (prostaglandin E, etc.) inhibit the release of mediators. Antagonistic relationships are also characteristic of hormonal regulation. The inflammatory response is enhanced by pituitary somatotropic hormone (GH), deoxycorticosterone (reticular zone) and aldosterone (glomerular zone) of the adrenal cortex, while glucocorticoids of the adrenal bundle zone weaken it. Cholinergic compounds (acetylcholine, etc.) have a pro-inflammatory effect, which accelerate the release of mediators, and vice versa, adrenergic substances (adrenaline and noradrenaline of the adrenal medulla, corresponding nerve endings), like anti-inflammatory hormones, inhibit the action of mediators.

Immune mechanisms significantly affect the course and outcome of the inflammatory response. With a high general resistance and immunobiological reactivity, the inflammatory reaction proceeds with the predominance of protective and adaptive processes and with a more complete restoration of damaged tissues. However, with prolonged antigenic stimulation (sensitization) of the body, an increased or excessive inflammatory reaction (allergic or immune inflammation) develops. The immunodeficiency state of the body with a decrease in the activity of protective mechanisms causes an unfavorable course and outcome of the inflammatory reaction.

MeaningandExodusinflammation. The significance of inflammation for the body is determined by the fact that this complex biological reaction, developed in the process of long evolution, has a protective and adaptive character to the effects of pathogenic factors. Inflammation manifests itself as a local process, but at the same time general reactions develop: the body mobilizes nerve and humoral connections that regulate the course of the inflammatory reaction; metabolic processes and blood composition change; functions of the nervous and hormonal systems; body temperature rises.

The nature and degree of manifestation of the inflammatory reaction are determined both by the etiological factor and the reactivity of the organism, its immunity, and the state of the nervous system. Hormonal and other systems. With which inflammation is inseparable unity. During the primary contact of an organism with normal immune properties with a pathogenic stimulus, normergic inflammation develops, which in manifestation corresponds to the strength of the stimulus. With repeated or repeated exposure to the body of an antigenic stimulus (sensitization), allergic (hyperergic) inflammation develops, which is characterized by pronounced alterative, exudative (immediate type hypersensitivity reaction) processes.

In an organism with reduced reactivity and an immunodeficiency state, weakened or severely depleted, there is a slight inflammatory reaction, hypoergic inflammation, or it is completely absent (negative energy). The lack of response in the presence of innate or acquired immunity is seen as positive energy. If inflammation occurs as a result of a violation of the normal course of immune reactions (with immunopathological reactions), then they speak of immune inflammation. Tin and the nature of inflammation depend on the type and age of the animal.

It is generally accepted that inflammation is a relatively expedient protective and adaptive reaction, the biological role of which is determined by the healing forces of nature, the struggle of the body with harmful pathogenic stimuli. The adaptive mechanisms of this reaction are not perfect enough, inflammation can be accompanied by an unfavorable course and outcome. The resulting inflammation must be managed.

Complete resolution of the inflammatory process, associated with the elimination of the pathogenic stimulus, resorption of dead tissues and exudate, is characterized by morphofunctional restoration (regeneration) of the structural tissues of the inflammatory process, associated with the elimination of the pathogenic stimulus, resorption of dead tissues and exudate, is characterized by morphofunctional restoration (regeneration) of structural tissue and cellular elements and organ in the area of ​​inflammation.

Incomplete resolution with incomplete recovery is observed in cases of prolonged persistence of a pathogenic stimulus in inflammatory tissues, in the presence of a large amount of exudate (especially purulent, hemorrhagic or fibrous), with significant damage and in highly specialized tissues with a special rhythm of functioning (central nervous system, heart muscle, large vessels, lungs), especially in weak and emaciated animals. At the same time, pathological conditions are noted in the focus of inflammation: atrophy, necrosis (including salt precipitation), stenosis or expansion (cysts) of the gland ducts, adhesions, adhesions, connective tissue scars, calluses and other processes that deform the organ.

At any stage of the inflammatory process, structural-functional and immune insufficiency of the inflamed organ can develop or loss of its functions with a fatal outcome can be observed. Of particular danger is inflammation of vital organs (brain and spinal cord, heart, lungs). In the presence of extensive lesions, traumatic or bacterial-toxic shock, sepsis and poisoning with toxicological decay products of dead tissue (autointoxication) develop.

Classificationinflammation. It is based on a number of principles.

I. Depending on the etiological factor, there are:

1) non-specific, or banal (polyetiological);

2) specific inflammation. Nonspecific inflammation is caused by various biological, physical and chemical factors, specific inflammation arises from the action of a certain, or specific, pathogen (tuberculosis, glanders, actinomycosis, etc.)

II. According to the predominance of one of the components of the inflammatory reaction, regardless of the cause, there are:

1) alternative (parenchymal);

2) exudative;

3) proliferative (productive). Depending on the nature and other features, each type is divided into forms and types. For example, exudative inflammation, depending on the type and composition of the exudate, is serous (edema, dropsy, bullous form), fibrinous (croupous, diphtheritic), purulent (abscess, phlegmon, empyema), hemorrhagic, catarrhal (serous, mucous, purulent, desquamative, atrophic and hypertrophic catarrh), putrefactive (gangrenous, ichorous) and mixed (seropurulent, etc.).

III. According to the course, there are: acute, subacute and chronic inflammation.

IV. Depending on the state of the body's reactivity and immunity, inflammations are distinguished: allergic, hyperergic (immediate or delayed hypersensitivity reactions), hypoergic, immune.

V. According to the prevalence of the inflammatory reaction: focal, diffuse, or diffuse.

6. Gangrenous and proliferative inflammation

putrid,gangrenous,ichorous ( from the Greek ichor - serum, ichor), inflammation. It is a complicated course of any exudative inflammation with putrefactive tissue decay. Observed in organs in contact with the external environment.

Causes are associated with the development of tissue necrosis in the focus of inflammation and the ingress of putrefactive microflora into them. This is facilitated by accidental entry of foreign objects into open organs, aspiration of vomit into the lungs, improper administration of medicinal substances, the use of insufficiently processed instruments, and violation of other sanitary rules.

Pathogenesis. It is determined by the presence of dead tissues in the focus of inflammation and the reproduction of putrefactive microflora. Animals with a weakened general resistance and an immunodeficiency state are predisposed to such complicated inflammation.

macroscopicchanges. They are characterized by the presence of putrefactive (gangrenous, ichorous) disintegration of tissues and ichorous mass in the lumen of the abdominal organ. The inflamed focus, and sometimes large areas of the organ (uterus, mammary gland) are black-brown or gray-green in color, the specific smell of decayed tissues soaked in ichorous fluid, sometimes with gas bubbles when anaerobic microflora is introduced (gas gangrene). Microscopic examination of the affected organ establishes the presence of characteristic signs of an exudative organ, establishes the presence of characteristic signs of exudative inflammation, complicated by progressive necrosis, the presence of colonies of microorganisms and blood pigments in dead tissues. Demarcation inflammation is usually mild. Most leukocytes with signs of karyopyknosis, rexis and lysis.

Putrid inflammation leads to the development of sepsis or autointoxication with a fatal outcome.

Polyferativetypeinflammation

Polyferative ( productive ) inflammation . It is characterized by the predominance of proliferation (from lat. Proles - offspring, offspring, fero - I carry), or reproduction, cellular elements, less pronounced and exudative changes. The productive process (from Latin producere - to produce) with the neoplasm of cellular elements proceeds in the following forms: interstitial (interstitial) inflammation and granulomatous inflammation.

Intermediate ( interstitial ) inflammation characterized by the predominant formation of diffuse cell proliferate in the stroma of the organ (liver, kidneys, lungs, myocardium, etc.) with less pronounced dystrophic and necrotic changes in parenchymal elements.

Similar Documents

Tasks facing specialists in ensuring the productivity of farm animals and preventing their diseases. Cattle keeping systems. Hygiene of the cellular content of chickens. Castration of farm animals.

test, added 09/17/2012


Anamnestic and clinical data. Analysis of the conditions for keeping pigs in a farming and peasant economy, animal feeding. The results of the external, the study of the internal organs of the mumps. The main pathological diagnoses, causes of death of the animal.

report, added 04/25/2012


The procedure and stages of veterinary and sanitary examination of the meat of forcedly slaughtered animals in case of poisoning, features and significance. Classification of meat depending on the degree of toxicity, the possibility of its use. Conducting a forensic veterinary autopsy.

test, added 04/27/2009


Infectious diseases of farm animals and birds. Morphology and chemical composition of the pangolin virus, clinical signs of the disease. Alimentary and respiratory routes of infection in animals, pathological changes and differential diagnosis.

term paper, added 12/11/2010


Drawing up an act of a forensic veterinary autopsy of a piglet. Conducting an external and internal examination of the corpse, making a diagnosis. Finding out the circumstances from which the animal fell, whether it was possible to save it. Methods of prevention of the detected disease.

term paper, added 08/19/2010


The concept and main content of the autopsy protocol, the procedure for its preparation, types of examination: external, internal. Clinical and anatomical analysis of the diagnostic case of the disease. The order and principles of the final diagnosis.

practice report, added 04/13/2014


The main systems of keeping farm animals and their characteristics. Hygiene of keeping pigs, sheep, horses and poultry. Sanitary and hygienic requirements for the site for the construction of livestock farms and complexes.

control work, added 08/02/2015


Veterinary services for animal husbandry in the Mostovsky district of the Krasnodar Territory. Characteristics of the place of autopsy of corpses and their disposal. Analysis of a diagnostic case of eimeriosis. Protocol for the pathoanatomical autopsy of a duckling.

term paper, added 08/19/2010


Principles of organization of veterinary business. Formation of livestock industries in the XIX and early XX centuries. The pace of development of animal husbandry. Training of veterinary specialists according to the type of Khoroshevskaya boarding school. Setting up veterinary education.

abstract, added 04/09/2012


Malnutrition as the main cause of metabolic disorders in farm animals. The occurrence of rickets in violation of mineral and vitamin metabolism in the body. Symptoms and course of the disease, its diagnosis and treatment.