Общая патологическая анатомия животных = Introduction to the pathological anatomy of animals. Учебно-методическое пособие

Liver damage.

Fatty liver dystrophy can occur in two types:

1.macrovesicular fat dystrophy

2.toxic (foamy, decomposition)

Macrovesicular hepatic steatosis

The liver is enlarged in volume, the capsule is tense, the edges are

roller-like, sometimes there are breaks in the capsule, the color at the beginning of the process is clay, then ochre-yellow. The liver is sticky, pasty consistency, easily torn by hands. When the incision on the skin and the hands is of fatty plaque. On the section picture of the liver is Muscat, as the process of obesity begins with the periphery of the hepatic lobule. It is lighter, which gives the liver a Muscat pattern.

Toxic fat dystrophy

It depends on the process. Dystrophy develops in two stages.

1.Stage of yellow atrophy of the liver. It is characterized by the accumulation of small drops of fat in hepatocytes, which leads to their atrophy.

2.The stage of red atrophy of the liver. There is atrophy and necrosis of hepatocytes, connective tissue comes to their place. It has a bright red color and is rich in vessels.

At the beginning of the process, the liver is increased in volume, clay-colored, easily torn by hands, the cut pattern is smoothed, the surface is sticky. Further on, as the growth of connective tissue and the formation of tissue regeneration nodes, the liver acquires a shagreen (finely-bumpy) surface, and then large nodes appear – areas of liver regeneration, between which the coarse-fibrous connective tissue is located.

Micro: when globular fatty degeneration, the process starts from the periphery of the liver lobules, there liver is infiltered by fat through the blood vessels of the triad.

Morphogenesis: first, hepatocytes are formed in the enlightenment of the cytoplasm, and then made into small fat droplets, which have a tendency to merging and consolidation. In the end, one huge drop of fat is formed, which fills the entire cytoplasm of the cell, leading to atrophy of the cytoplasm and the nucleus, shifting the nucleus to the periphery – a ring-shaped cell is formed.

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Toxic (foamy) fat dystrophy – the process begins with the center of the hepatic lobule, that is, toxins enter the liver through the central hepatic vein, which leads to the decomposition of cytoplasmic fats. The resulting fat droplets are very small, as a rule, they do not merge with each other. Cytoplasm of hepatocytes and liver tissue under a microscope become foamy.

Morphogenesis: stage of yellow liver atrophy: initially, in hepatocytes located in the center of the hepatic lobule, cytoplasmic enlightenment is formed, which quickly deform and turn into small drops of fat. They quickly fill the entire cytoplasm of the cell, leading to the disintegration of the nucleus, and to the death of hepatocytes. Stage of red atrophy: then young cells of connective tissue – fibroblasts come to their place, which, when ripe, give rise to fibrous scar structures.

Clinical value: in case of large-scale fat dystrophy, the function of the organ only slightly decreases, after the cessation of the pathogenic factor, everything comes to normal. With toxic fat dystrophy, cirrhosis of the liver develops, which leads to liver failure.

Violation of carbohydrate metabolism. Carbohydrate dystrophy

These dystrophies are very rare in animals. It is characterized by changes in the amount of glycogen in the tissues. Glycogen is found in tissues in stable form – bound to proteins and in labile form – not protein-bound. The main reserves of glycogen are contained in the liver and skeletal muscles.

Etiology: metabolic disorders and endocrine system disorders. Macroscopically, carbohydrate dystrophy is not recognized. Micro: when stained with Schiff's reagent (PAS-reaction) increase

or decrease in the content of glycogen in tissues is noted.

Clinical value: violation of energy metabolism, as glycogen is a reserve of rapid mobilization of energy substrates.

Violation of mineral metabolism

By the value for the body all the minerals are divided into macro-, micro - and ultraelements. The main role of minerals is to participate in metabolism. They are parts of enzymes, hormones, vitamins, pigments, plastic substances, etc.

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From the point of view of pathology, the most important is the violation of calcium metabolism.

Violation of calcium metabolism – calcareous degeneration

Synonyms: calcification, petrification, calcium thesaurismosis. The essence of the process: calcium salting of tissues.

The mechanism of calcareous degeneration:

1.metastatic calcification

2.dystrophic calcification

3.metabolic calcification

Metastatic calcification

Formation of lime metastases. This process is associated with

hypercalcemia and is manifested by the deposition of calcium salts in the kidneys, myocardium, lungs, gastric mucosa, in the walls of arteries. Here are found grains of calcium salts, which are brought by the flow of blood.

Dystrophic calcification – petrification

This is a local process of deposition of calcium salts in dead dystrophic changed dramatically scleroid tissues.

Mechanism: the pH of the altered tissues is acidic, therefore, moving from the alkaline medium of the blood, calcium is connected to acidic ions and calcium salts fall into the tissue. This process is observed in severe inflammation, necrotic lesions, inflammation with the formation of granules, helminthosis.

Metabolic calcification – calcification

System or local process of calcium salts deposition as a result of deep disturbance of mineral metabolism.

Pathomorphology depends on the degree of severity of the process. The appearance of the tissue, impregnated with calcium salts, at the beginning of the process is almost unchanged. In far-gone cases, the tissue is badly cut with a knife, crunched, creak when cut, on the surface of the cut hard or loose grains or lumps of gray-yellow or white are exposed.

Micro: calcium salts are basophilic, i.e. stained by hematoxylin in dark purple color. They can be found in the center of necrosis foci, in old inflammation foci, in abscess capsules, in the wall of arteries, skin, etc.

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Pathomorphology of nosologic units related to the violation of calcium metabolism

1. Fibrous degeneration

This is a common or local pathology associated with resorption of bone tissue and its replacement by fibrous.

Etiology: hypertrophy of the parathyroid gland, imbalance of protein and calcium diets, hypo - and avitaminosis of A and D, metabolic disorders of proteins and carbohydrates.

Pathomorphology: pathology is localized most often in the bones of the skull, ribs, limbs. There is a softening of bone tissue, then the growth of the bone tissue of coarse-fiber connective tissue with further formation of scar tissue (sometimes connective conglomerates are formed).

2. Halisteresis (osteomalacia)

A serious disease associated with a violation of calcium metabolism and characterized by leaching of calcium from the bones and their resorption. It is observed most often in adult animals, most often in ruminants.

Etiology: errors in feeding (acidic food) and metabolic disorders (impaired buffer systems of blood).

Pathomorphology is characterized by thinning of bone tissue, its fragility, the emergence of spontaneous fractures.

Micro: thinning of the bone beams and their atrophy.

3. Rickets

Severe disease of young animals associated with a violation in animal feeding, with a lack of UV radiation and vitamins A and D3 and a lack of calcium.

Pathomorphology: there is underdevelopment of bone tissue, disproportion of body parts, the bones are softened and easily cut with a knife, on the ribs rickets beads are formed – thickening of bone tissue.

Clinical value depends on the degree of severity of the process and is a deep violation of not only mineral but also all kinds of metabolism in the flesh to the death of the body.

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Stone formation (lithiasis) – concretion

Calculus is dense formations, lying freely in natural cavities or tissues of the body and having in its composition calcium salts, desquamated descended cells, undigested feed residues, foreign bodies, hair, etc.

Etiology:

1.decrease or increase in salt content in the body

2.inflammation of natural cavities

3.changes of colloidal state of secrets

4.metabolic disorder

Feature: composition, size, shape, color of stones, is variable and depends on the type of animal, age, conditions and place of formation of stones.

Gastrointestinal concretions

Can be true and false. True (enteroliths) are 90% or more composed of calcium salts, they are solid as a stone, they have a layered structure on the cut, which indicates their gradual formation, that is, the layering of calcium salts in the form of an onion. In the center of the enteroliths are often dead cells or a foreign body.

False concrements of gastrointestinal system (pseudoenterolites) consist of organic matter mixed with mineral salts. Such pseudoenterolites are distinguished;

1.fitoconcrements – remains of vegetable fibers impregnated with salts of calcium.

2.proconcrete – hair impregnated with calcium salts.

3.conglobates-formed in the large intestine.

Uroliths

These are the stones formed in the body with KSD. This disease is polyetiological and includes metabolic disorders, feeding errors, inflammation of the kidneys and urinary tract, violation of the colloidal composition of body fluids, parasitic diseases. With the formation of uroliths of different composition appear. It can be urates-salts of uric acid, oxalates-salts of oxalic acid, phosphates-salts of phosphoric acid, calcareous forms of stones, etc.

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Gallstones

They are formed in liver tissue, but most often in the gallbladder. They have in its composition proteins, bile acids, cholesterol and calcium salts. Their consistency, size, color are completely different.

Etiology: polyetiological disease.

Stones of salivary glands

In the salivary glands sialolites are formed. It is a group of dead cells impregnated with calcium salts. They are located in the salivary ducts, clog them, which leads to atrophy of the salivary glands.

The outcome and value for organism: various. Many stones are found in the slaughter or after the death of the animal. In gallstone disease – mechanical jaundice, with stones of the salivary glands – atrophy of the salivary glands.

Necrosis

Necrosis is the death of cells of a tissue or even a whole organ, but in a living macroorganism. The nature of the necrosis is complete and irreversible termination of vital activity of a tissue.

There are two types of cell death in tissues:

1.physiological programmed death – apoptosis.

2.pathological death – necrosis.

The essence of apoptosis is that the cell prepares for death and eliminates potentially dangerous organelles (primarily lysosomes). Therefore, the death of the cell in apoptosis does not have any consequences for the tissue.

The essence of necrosis is pathological cell death under the influence of pathogenic factor – the cell is not preparing for its death, so the development of necrosis causes changes in the tissue, in particular, perifocal inflammation or other forms of inflammatory reactions.

Necrosis undergoes a number of stages in the process of its development, which suggests the morphogenesis of necrosis.

Necrosis morphogenesis includes 4 stages:

1.Paranecrosis is severe, but reversible dystrophic changes in the tissues.

2.Necrobiosis is an irreversible degenerative changes in the tissues.

3.Actual necrosis the death of a cell or a tissue.

4.Autolysis is decomposition of dead sybstrate.

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Etiology of necrosis

These are mechanical, physical, chemical, biological factors, CNS lesions, circulatory disorders and other pathogenic effects that exceed the force of the adaptive and compensatory tissue capabilities. In this regard, etiologically two groups of necrosis are distinguished:

1.Direct necrosis.

2.Indirect necrosis.

Direct necrosis is the death of tissues directly at the site of application of a pathogenic factor or agent. For example, necrosis as a result of chemical factors (acid).

Indirect necrosis is the necrosis of tissues when the focus of necrosis is formed somewhat remotely from the site of application of the pathogenic agent. For example, neurotrophic ulcers, heart attacks, etc.

Morphological classification and characteristics of necrosis The appearance of the necrosis focus varies depending on:

1.reasons

2.tissues

3.reactivity

Most often, the focus of necrosis is gray-white or gray-yellow. With stagnation a focus of necrosis will be dark red or even black

because of a change hemoglobinogenic pigments. In the intestine, the focus of necrosis can be impregnated with bile, which gives the necrosis a greenish hue. Necrosis of the skin due to the formation of sulfur iron will be black.

The consistency of the dead substrate can be:

1.Dense or similar to dried cottage cheese

2.Soft, smearing, gruel-like

In this regard, there are three types of necrosis:

1.Coagulative – dry (a kind of caseous necrosis)

2.Colliquative – wet

3.Gangrene

Coagulative necrosis

It is a dry necrosis that develops in tissues that are rich in proteins, as a result of clotting of tissue proteins and rapid return of moisture by tissues. The inflow of blood in the tissue is difficult.

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Macroscopically: the focus of necrosis is gray-yellow-white, necrotic masses are dense, dryish, the pattern of the organ is blurred from the surface and on the section. A kind of dry necrosis is caseous necrosis - with glanders and tuberculosis. Necrotic masses at the same time resemble dried cottage cheese.

Colliquative necrosis

Wet necrosis, developing in tissues rich in moisture. It can be brain, bone marrow, intestine, lungs. There is a softening of necrotic masses, up to the slurry or even emulsion. The liquid enters the focus of necrosis with blood and due to autolysis. Example: softening of brain tissue, wet necrosis of the intestine up to the perforation of the intestinal wall.

Gangrene

It is the necrosis of the tissue that touches the external environment. Feature: this is the most severe form of necrosis, as the tissue is, inter alia, exposed to air, temperature, infection, etc. Under the influence of these factors the color of the foci of gangrene dirty-brown, gray-green or even black. Distinguish gangrene dry, wet and gas

(noisy).

Dry gangrene is most often localized in the skin. Gangrene focuses are black due to the formation of sulfurous iron. Dry gangrene accompanies chronic erysipelas, leptospirosis, and bedsores.

Wet gangrene (septic, putrid) develops under the influence of putrid microorganisms. The focus of the gangrene is dark, up to black, the consistency is soft, decaying, stinking. A typical example is lung gangrene (when aspiration of feed, liquid or under the influence of putrefactive microorganisms).

Gas (noisy) gangrene develops under the influence of anaerobic microflora, which, developing in the tissues, leads to necrosis, but the fabric is impregnated with gas bubbles. A typical example is emphysematous carbuncle, malignant edema and other clostridiosis. The fabric is impregnated with gas bubbles.

Microscopically necrosis is manifested by changes in the nucleus and cytoplasm of the cell. Kernel necrosis when the first one dies. There are three types of changes:

1. karyopyknosis – condensation, compaction and shrinkage of the nucleus.

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2.karyorhexis – decay of the nucleus into individual chromatin fragments.

3.karyolysis - decay of the nucleus.

The cytoplasm if necrosis is subjected to cytopic disease, cytorexis, cytolysis (disintegration into fragments), cytolysis (disintegration). After cytolysis and karyorhexis in the focus of necrosis by the debris of cells and cellular detritus are formed.

In general, necrotic masses are oxyphilic and the focus of necrosis is homogeneous or grainy light pink masses, with separate inclusions of nuclear debris.

Released lysosomal and other enzymes in cell necrosis initiate the development of borderline perifocal inflammation. Borderline inflammation is a cell shaft with hyperemic vessels, the main function of which is to protect relatively healthy tissue from the effects of necrotic masses. The cellular composition of perifocal inflammation is represented by epithelioid, lymphoid cells, neutrophils, macrophages. As the cell structure matures, it gives way to the young elements of connective tissue – fibroblasts and eventually forms a fibrous connective tissue. That is, a capsule is formed around the focus of necrosis.

Atrophy

Atrophy is a lifetime reduction of cells, tissues, organs with weakening of their functions. In the organ, both parenchyma and stroma are proportionally reduced.

The pathogenesis is determined by a gradual decrease in the intensity of metabolic processes, which leads to a decrease in the number of cells in the tissue, both in the parenchyma and in the stroma.

The most sensitive to external factors, and therefore the most susceptible to atrophy parenchymal organs, built of highly differentiated cells and tissues.

The atrophic process always develops slowly, which indicates the chronic course of the disease, or the chronic effects of factors that cause atrophy.

Atrophy is both local (affects the organ or tissue) and general (cachexia). According to the value for the body atrophy can be physiological and pathological.

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Physiological atrophy is a pattern of physiological processes that occur in the natural development of the body. This includes periodic atrophy (molting, involution of the breast after lactation, involution of the uterus after childbirth, senile atrophy, atrophy of the thymus during puberty).

Pathological atrophy occurs under the influence of various pathogenic factors, it is classified according to the etiological principle:

1.Pathological atrophy from the influence of physical factors - from the action of pressure (compression atrophy, atrophy from the effects of x-rays, electric rays, etc.)

2.Pathological atrophy from the effects of chemical factors (lack or excess of trace elements, the action of poisons and toxins, unbalanced diet)

3.Hormonal pathological atrophy-observed in the defeat of the endocrine glands, for example, hyperthyroidism, pituitary gland leads to cachexia.

4.Neurotic (neurogenic) pathological atrophy develops as a result of a violation of the nervous trophic disease, for example, when a nerve is damaged or bruised, etc.

5.Functional pathological atrophy – atrophy from inaction (with paresis, paralysis, etc.)

6.Pathological atrophy from starvation

Signs of atrophy

There are five signs of atrophy:

1.Changes in the volume and weight of the body – they are usually reduced. In the liver, the spleen edges thin, they become leathery, the pattern of the body from the surface is more clearly visible. Sometimes the volume and weight of the body can be increased due to the growth of connective tissue (CT) or fat, or the accumulation of other substances (air, liquid, etc.). For example, atrophy in colloidal goiter, emphysema, hydronephrosis.

2.Changing the color of the body – the color of the body is paler than usual due to anemia. Afterwards because of the growth of CT or fatty tissue the organ can become of grey-white-yellow color. Muscle, myocardium, liver coloration may acquire a brownish tinge in connection with the accumulation of the pigment lipofuscin.

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