Veterinary pathological anatomy. pathological anatomy
Pathological morphology, the science of the development of structural changes in a diseased organism. In the narrow sense, under P. a. understand the study of macroscopic. changes in an organism, unlike patol. histology and patol. the cytology revealing patol. processes methods microscopy and histochemical. research. As an academic discipline P. a. subdivided into the general, studying types patol. processes, regardless of the etiology of the disease, the type of animal and the affected [stricken] organ (necrosis, dystrophy, inflammation, etc.), organopathology, which studies the same processes depending on their localization, and special. P. a., exploring the complex of changes in a particular disease. Organopathology and special P. a. sometimes united in private P. and. Sources of material for studying P. a. - autopsy, biopsy, organs of experimental animals. P. a. closely related to pathological physiology , together with a cut makes a science about a sick organism - the pathology which is the base for honey. and vet. Sciences.
The emergence of P, a. associated with the development of anatomy and physiology. The founder of P. a. - Italian. doctor J. Morgagni (1682-1771), who connected the disease with the anatomical. changes in organs. All R. 19th century cellular pathology arose (R. Virchow), which determined painful changes at the level of cells and tissues. P. a. animals began to develop rapidly from the 2nd floor. 19th century Prominent scientists abroad [scientists] in the field of vet. P. a.; in Germany - T. Kitt, E. Yost, K. Nieberle; in Romania - V. Babesh; in Hungary - F. Gutira, J. Marek and others. The beginning of the development of vet. P. a. in Russia, laid the work of I. I. Ravich, A. A. Raevsky, N. N. Mari. The largest owls pet. pathologists - K. G. Bol, N. D. Ball and many of them. students - B. K. Bol, B. G. Ivanov, V. Z. Chernyak and others.
P, a. animals develops as a science, one with P. a. person. The work of owls. pathologists studied morphological. changes and their development at the majority of diseases of page - x., pets, commercial mammals, birds and fishes that matters for knowledge of essence of diseases, their diagnosis and check of efficiency to lay down. events. Special attention vet. pathologists devote to the study of the pathomorphogenesis of infections. animal diseases, in particular viral, malignant. tumors, metabolic diseases; dynamics of reparative processes, taking into account [taking into account] physiol. animal status; embryonic pathology in various animal species; morphology of the general patol. processes at the molecular and submolecular levels, etc.
Teaching vet. P. a. carried out on a special departments in vet. in-ta and technical schools. Pathological anatomical departments and laboratories exist at all n.-and. vet. in-tax and diagnostic. laboratories.
In 1960, a section of veterinarians was organized. pathologists in the All-Union Society of Pathologists.
Lit .: Pinus A. A., From the history of the development of veterinary pathological anatomy in pre-revolutionary Russia, in the book: Tr., All-Union Interuniversity Scientific and Methodological Conference on the pathological anatomy of agricultural. animals, Voronezh, 1961; Pathological anatomy of page - x. animals, floor ed. K. I. Vertinsky, N. A. Naletova, V. P. Shishkov. Moscow, 1973.
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- 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 peeled 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 with 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 flows freely 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).
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. In this case, 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. The 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, of 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 limb stump 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 repeated 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 scar formation. 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 a 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 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.
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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 and others.
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.
Material and research methods
In pathological anatomy, the following materials and research methods are used: autopsy, pathomorphological examination of carcasses and organs of forcedly slaughtered animals, biopsy methods during surgical operations and experimental.
Autopsy of corpses is the main research method.
The biopsy method is the taking of pathological material (biopsy) during life and its study.
Experimental method - to obtain a model of the disease in an experiment in order to study the dynamics of the morphogenesis of the pathological process or evaluate new therapeutic or preventive measures.
Research methods are divided into macroscopic (visual) and microscopic.
Scheme for describing compact organs (liver, kidneys, lungs, spleen, etc.):
The size (volume, weight) is determined by the condition of the edges, the tension of the capsule and the swelling of the parenchyma from the cut capsule or by the results of measurement and weighing;
Shape (general view and outline, ratio of parts of the nature of the edges: sharp, blunt, rounded);
Surface (color, transparency, degree of filling of blood vessels, surface moisture, surface shape, elevation and depressions, gloss, turbidity, overlays);
Consistency (organ as a whole, individual parts of sites or nests);
View of the cut surface (drawing of the structure, the nature of the flowing liquid).
Scheme for describing abdominal organs (stomach, intestines, etc.):
The position of the organ (normal or displaced);
value;
Mucosa (thickness, type, color, nature of the secret).
The state of the submucosal layer, muscular and serous membranes.
Scheme for describing the serous cavities (abdominal, thoracic and cardiac membranes):
The position of the organs in the cavity (normal or displaced);
Foreign content (quantity, transparency, color, smell, composition);
Serous membranes - peritoneum, pleura, epi- and pericardium (moisture, dryness, shine, color, smoothness, the presence of overlays and adhesions).
Microscopic studies.
Examination of histological preparations under a microscope:
Making histological sections;
Examination of histological preparations under a microscope.
Death and post-mortem changes in the body, their differential diagnosis from intravital changes
Death as a biological concept is an irreversible cessation of metabolism and vital functions of the body. A decrease in the intensity of the metabolism and vital activity of the body to an almost complete suspension is called suspended animation.
Death is the inevitable end of the natural life cycle of any organism. With the onset of death, a living organism turns into a dead body, or corpse.
The life span of animals of different species is different and depends on the natural (phylogenetic, hereditary) features and conditions of existence.
Etiology of death
The natural, or physiological, death of the body occurs in extreme old age as a result of its gradual wear and tear. There are various theories of aging and death: the immunological theory and the theory of somatic mutations, the theory of autointoxication, the theory of neuroendocrine regulation disorders with a decrease in the efficiency of inductive enzyme synthesis and the development of irreversible metabolic abnormalities.
However, higher animals die much earlier than their natural physiological lifespan due to disease, inability to obtain food, or external violence.
Death from exposure to pathogenic causes (exogenous or endogenous aggressive stimuli) is pathological (premature). It is non-violent and violent. Distinguish non-violent ordinary death from diseases with a clinically pronounced manifestation and sudden death (sudden) without visible harbingers of death, which occurred unexpectedly in apparently healthy animals.
Violent death(unintentional or intentional) is observed as a result of such actions (unintentional or intentional) as murder or murder, death from various kinds of injuries (for example, work injury), accidents (transport accident, lightning discharges, etc.).
Death process (thanatogenesis)
Conventionally, it is divided into three periods: agony, clinical (reversible) and biological (irreversible) death.
Agony - the process from the beginning of dying to clinical death - can last from a few seconds to a day or more. Clinical signs of agony are associated with a deep dysfunction of the medulla oblongata, uncoordinated work of homeostatic systems in the terminal period (arrhythmia, pulse fading, convulsions resembling a struggle, paralysis of sphincters). The senses of smell, taste, and last but not least, hearing are gradually lost.
Clinical death is characterized by a reversible cessation of vital body functions, respiratory and circulatory arrest. It is determined by the primary clinical signs of death: the last systole of the heart, the disappearance of unconditioned reflexes (determined by the pupil), the absence of encephalogram indicators. This extinction of the vital activity of the organism is reversible under normal conditions within 5-6 minutes (the time during which the cells of the cerebral cortex can remain viable without oxygen). At low temperatures, the time of experiencing the cerebral cortex increases to 30-40 minutes (the deadline for people to return to life when they are in cold water). In terminal conditions (agony, shock, blood loss, etc.) and clinical death, a set of resuscitation measures is used to restore the functioning of the heart, lungs and brain.
Biological death is the irreversible cessation of all vital functions of the body with the gradual death of cells, tissues, and organs. After the respiratory and blood circulation stops, the nerve cells of the central nervous system are the first to die, then the cells of the endocrine and parenchymal organs (liver, kidneys) die. In other organs and tissues (skin, heart, lungs, skeletal muscles, etc.), the process of death continues for several hours or even days, depending on the ambient temperature and the nature of the disease. During this time, despite the destruction of cell ultrastructures, the general structure of many organs and tissues is preserved, which makes it possible to determine the nature of intravital pathological changes and the causes of death during postmortem autopsy and anatomical examination. Cardiac and respiratory arrest are the closest signs of death. Thanatology, which led to cardiac and respiratory arrest, are the defining signs of death.
Determining the causes of death is the responsibility of doctors, including pathologists and forensic experts. Distinguish between the main (determining) and immediate (proximate) causes of death. The underlying cause is the underlying disease and the other causes mentioned above which, by themselves or through complication, cause the death of the animal. The immediate causes related to the mechanism of death (thanatogenesis) are associated with the cessation of the functions of the main organs that determine the vital activity of the organism. these include: paralysis of the heart, paralysis of the respiratory center and general paralysis of the central nervous system (cessation of brain activity). the conclusion is made on the defining signs of death.
After the onset of biological death, secondary and tertiary post-mortem physical and chemical changes develop (the primary signs of death include symptoms of clinical death). Secondary signs of death are changes associated with circulatory arrest and cessation of metabolism: cooling of the corpse, rigor mortis, cadaveric drying, redistribution of blood, cadaveric spots. Tertiary signs appear in connection with cadaveric decomposition.
Corpse cooling
After death, changes develop in the corpse, which are called post-mortem changes. After the death of the animal, the temperature of the corpse cools relatively quickly in a certain sequence to the ambient temperature. First of all, the ears, skin, limbs, head, then the trunk and internal organs are cooled. The rate of cooling of the corpse depends on the ambient temperature, air humidity and speed of its movement, the weight and fatness of the dead animal, as well as the nature of the disease and the cause of death.
At an external temperature of +18°C, cooling is 1°C per hour. If the animal died from infectious-toxic diseases (sepsis, anthrax) or with a predominant lesion of the central nervous system, the presence of convulsions (rabies, tetanus, brain injury, sun and heat stroke, strychnine poisoning, etc.), then after death the corpse is heated to 42°C, and then rapidly cooling it at 2°C per hour.
The cooling of the corpses of emaciated animals, young animals accelerates during bleeding. In a number of diseases, body temperature drops even before death occurs. At an ambient temperature of about 18 ° C, complete cooling occurs in the corpses of small animals (pigs, sheep, dogs) after about 1.5-2 days, and in large animals (cattle, horses) - after 2-3 days.
The degree of cadaveric cooling is determined by touch, and if necessary, measured with a thermometer. Its definition makes it possible to judge the approximate time of death of the animal, which is of practical importance in forensic veterinary autopsies and serves as one of the diagnostic features.
Rigor mortis
This condition is expressed by post-mortem compaction of the skeletal, cardiac and eye muscles, neck muscles and, in connection with this, the immobility of the joints and the unnatural position of the neck. In this case, the corpse is fixed in a certain position.
Rigor mortis is associated with biochemical processes in muscle tissue. The glycogen in them breaks down with the formation of lactic acid. In this regard, there is a softening of the muscle tissue. As lactic acid builds up in the muscles, the muscles harden and the joints become immobile. It is necessary to differentiate rigor mortis from intravital convulsions. When a limb is pulled from a corpse or the rigor is forcibly broken, the limb or head either returns to its original position. In rigor mortis, these parts of the body do not return to their original state.
Rigor mortis also affects the muscles of the internal organs. In the heart muscle, it can be expressed already after 1-2 hours. after death.
The onset time, duration and intensity of rigor mortis depend on the in vivo state of the organism, the nature of the disease, the causes of death and environmental conditions. Rigor rigor is strongly pronounced and sets in quickly in the corpses of large animals with well-developed muscles, if death occurs during hard work, from severe blood loss, with convulsions (for example, with tetanus, rabies, poisoning with strychnine and other nerve poisons). With injuries and hemorrhages in the brain, the deadly effects of electricity, rapid rigor mortis of all muscles (cadaveric spasm) occurs. On the contrary, rigor mortis sets in slowly, is weakly expressed or does not occur in animals with poorly developed muscles and in newborn hypotrophic patients, emaciated or dead from sepsis (for example, anthrax, erysipelas, etc.), in those who have been ill for a long time. Dystrophically altered skeletal muscles and heart muscles also undergo weak rigor mortis, or it does not occur at all.
Low temperature and high humidity of the environment slow down the development of rigor mortis, high temperature and dry air accelerate its development and destruction.
In diagnostic terms, the speed and degree of development of rigor mortis allow us to judge the approximate time of death, possible causes, circumstances, and the environment in which death occurred (corpse posture).
cadaveric desiccation
It is associated with the cessation of vital processes in the body and the evaporation of moisture from the surface of the corpse. First of all, the drying of the mucous membranes and the skin is noted. The mucous membranes become dry, dense, brownish in color. With drying, clouding of the cornea is associated. Dry gray-brown spots appear on the skin, primarily on hairless areas, in places of maceration or damage to the epidermis.
Post-mortem desiccation must be differentiated from intravital dehydration of the body, which often develops as a result of diarrhea or water starvation. With post-mortem drying, dryness is noted only in the visible mucous membranes, muscles and other surfaces of the body, however, the serous integuments of the abdominal cavity and other cavities are moist, shiny, and there is a small amount of liquid in the cavities. With dehydration, external signs of drying are found in combination with the dryness of the serous integument of the cavities and the absence of fluid in them.
Post-mortem blood clotting
The redistribution of blood occurs after death as a result of the postmortem contraction of the muscles of the heart and arteries. This removes blood from the heart. The heart, especially the left ventricle, becomes tight and constricted, the arteries almost empty, and the veins, capillaries, and often the right heart (with asphyxia) are overflowing with blood. A heart with dystrophic changes in the muscle does not undergo rigor mortis, or it is weakly expressed. In these cases, the heart remains relaxed, flabby, all its cavities are filled with blood. Then the blood, due to physical gravity, moves to the underlying parts of the body and organs. With the development of hypostatic hyperemia in the veins and cavities of the right half of the heart, the blood coagulates due to post-mortem changes in its physical and chemical state. Post-mortem blood clots are red or yellow or gray in the long agonal stage. They are elastic with a smooth surface, easily removed from the vessels, repeating the structure of the cavity in which they lie, in contrast to intravital thrombi, which are dryish, brittle and the head is firmly connected to the intima of the vessels. When they are removed, defects in the intima of the vessels are formed.
cadaveric spots
Arise in connection with the redistribution and changes in the physico-chemical state of the blood in the corpse. They appear 1.5-3 hours after death and up to 8-12 hours are in two stages: hypostasis and imbibition. Hypostasis is the accumulation of blood in the vessels of the underlying parts of the corpse and internal organs, therefore, external and internal hypostases are distinguished. At this stage, the cadaveric spots are dark red in color with a bluish tinge, are not clearly defined, turn pale when pressed, and drops of blood appear on the surface of the incision. When the position of the corpse changes, the spots can move. Cadaverous spots are well expressed in death from asphyxia, in plethoric animals and in other diseases with general venous congestion, when the blood does not coagulate. With anemia, exhaustion and after slaughter with exsanguination, hypostases are not formed. As a rule, they occur on the side on which the corpse lies. Cadaveric spots must be differentiated from intravital bruising and circulatory disorders. Cadaverous spots do not have sharply defined boundaries, as if fading away. When cut, tissue fluid protrudes, not blood. With intravital bruising, the epithelium of the skin is somewhat swollen; when cut, you can see a small amount of blood in the tissues. Cadaveric hypostases, as a rule, are located on the side on which the corpse lies and diffuse red staining of the tissues is distinguished, with hyperemia, the tissues are somewhat swollen and a network of vessels overflowing with blood is visible.
Stage of imbibition
It begins with the formation of late cadaveric spots after 8-18 hours or later - by the end of the first day after death, depending on the ambient temperature and the intensity of cadaveric decomposition. In connection with post-mortem hemolysis, the sites of early cadaveric spots are saturated with hemolyzed blood diffusing from the vessels. There are late cadaveric spots, or cadaveric imbibition. These spots have a pink-red color, do not change when pressed with a finger, a change in the position of the corpse does not cause them to move. In the future, cadaveric spots acquire a dirty green color due to the decomposition of the corpse.
Cadaveric spots can serve as a diagnostic sign of the disease, the absence of bleeding during slaughter in the agonal state, indicate the position of the corpse at the time of death. External cadaveric spots are detected on the surface of the skin. In animals with pigmented skin and thick hair, they are determined by the state of the subcutaneous tissue after skin removal.
cadaveric decomposition
Associated with the processes of autolysis and putrefaction of the corpse.
This process develops immediately after the death of the animal, but not simultaneously in different organs and tissues, but as structural elements are destroyed. The rate and degree of development of cadaveric autolysis depend on the number and functional state of the corresponding organelles in the cells, the number of proteolytic and other enzymes in the organs, the fatness of the animal, the nature of the disease and causes of death, the duration of the atonal period, and the ambient temperature. In the brain and spinal cord, glandular organs (liver, pancreas, kidneys, mucous membrane of the gastrointestinal tract, adrenal glands), it occurs faster.
Putrefactive enzymatic processes quickly (by the end of the first day) join the post-mortem autolysis due to the multiplication of putrefactive bacteria in the intestines, upper respiratory, genitourinary tract and other organs associated with the external environment, and their subsequent penetration into the blood of the entire corpse. As a result of putrefactive decay, cellular and tissue elements completely lose their structure.
Ultimately, as the corpses decompose, the consistency of the organs becomes flabby, a foaming liquid appears, and the organs turn into a fetid, dirty, gray-green mass. At the end of decomposition, the organic matter of the corpse undergoes mineralization and turns into inorganic matter.
It is necessary to differentiate post-mortem tissue autolysis from a pathological intravital process. Dead tissues in the corpse of animals undergo autolysis under the influence of digestive juices and enzymes, especially the mucous membranes of the digestive tract. Post-mortem erosions and ulcers appear, up to perforation of the wall of the stomach or intestines. Unlike intravital, they are presented as a defect without a vascular reaction at the site of erosion or ulcers. When food or feces fall out through the holes of the damaged areas on the serous membranes of the intestine or abdominal wall, they are easily washed off with water and remain shiny without change.
With intravital erosion (superficial lesion of the mucosa) or ulcers (deep damage to the walls up to the serous integuments), as a rule, the bottom and edges of them are uneven, swollen, reddened. When food or feces fall out through a perforated ulcer into the abdominal cavity, it causes inflammation of the serous cavities. Feed or feces are difficult to wash off from the serous cavities; when they are removed, a rough, inflamed surface remains.
Post-mortem bloating, caused by the multiplication of microflora after the death of the animal, must be differentiated from intravital bloating (tympania, flatulence, acute expansion). With post-mortem swelling of the stomach, intestines, blood vessels of the serous integument are overflowing with clotted blood, and there is no redistribution of blood in the body.
In intravital swelling, blood from the vessels of the serous integument of the stomach, intestines is squeezed out, they are pale. In addition, there is a redistribution of blood in the corpse of an animal: hyperemia of the skin of the underlying parts of the body, visible mucous membranes, anemia of the liver and spleen, and pulmonary edema, accompanied by foamy discharge from the nasal and oral openings.
Post-mortem rupture of organs or tissues must be differentiated from intravital, with it the edges of the rupture are even, there are no hemorrhages. In vivo - the edges of the gap are swollen, uneven, saturated with blood and there is always some amount of clotted blood.
test questions
- What do you know about the lifespan of different animal species?
- What are the theories of aging and death?
- What is the accepted classification of causes of death and stages of thanatogenesis?
- What are the immediate and defining signs of death?
- How to distinguish intravital injuries from post-mortem?
- On what grounds do conclusions are drawn about the causes of death of animals?
- What is the significance of atonal and cadaveric changes in pathoanatomical diagnostics and forensic veterinary examination?
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