Общая патологическая анатомия животных = Introduction to the pathological anatomy of animals. Учебно-методическое пособие
.pdfCell organelles and their changes in pathological conditions
Nucleous
The following nuclear changes are observed in the pathology:
1.Shape change (with heavy infections, toxicosis)
2.Size change (tumor growth, toxicosis)
3.Changes in the number of nuclei and nucleoli (hereditary pathology, radiation pathology, severe endotoxicosis-uremia)
4.Swelling of the nucleus (in toxicosis)
5.The presence of intra-nuclear bodies-inclusions (more often in viral infections-plague, parvovirus enteritis, rabies, etc.)
6.Pathologies of nuclear shells, such as delamination, breaks, disappearance of the structure of one of the layers.
In general, in severe cases, changes in the core are manifested in the form:
A. Karyopyknosis – shrinkage of the nucleus;
B. Karyorhexis – decay of the nucleus into pieces; B. Karyolysis - dissolution of the nucleus.
Cytoplasm
Changes in cytoplasm are associated with changes in cell organelles, as well as violation of the microtubules and transport network. In this case, there is condensation and denaturation of cytoplasmic protein, as well as the accumulation of fat drops, water drops or other inclusions. All in all, changes in cytoplasm in severe cases are expressed as:
A.Citopic disease – wrinkling
B.Cytorexis – disintegration of the cytoplasm into fragments
B.Cytolysis-dissolution of the cytoplasm
Endoplasmic reticulation (EPR)
EPR changes are manifested mainly in the form of reduction or increase in the number of ribosomes, as well as violations of the state of endoplasmic transport. All this leads to bogging of cells and their swelling, which leads to death. The increase in the number of ribosomes and structural membranes of EPR indicates the development of hypertrophic processes in the cell, and the decrease – about atrophic processes.
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Mitochondria
These are the most labile cell organelles; they are the first to be involved in the development of the pathological process. The most common changes are met in mitochondria:
1.Condensation – grouping of the mitochondria
2.Swelling
3.The appearance of inclusions in the mitochondria
Most often, all three processes go simultaneously. The intimate mechanism of development of these processes – any influences leading to development of hypoxia.
Lysosomes
This kind is of killer cells, as they contain a huge number of lytic enzymes, primarily proteolytic. The slightest damage to the membrane of the lysosome leads to the destruction of it and the outpouring of content in the cytoplasm, leading to cell lysis. The destruction of lysosomes is caused by toxins, hypoxia, starvation, mechanical injuries, shock, carcinogens and other factors.
The most labile tissue in the body is the epithelium. It is the first to suffer. Then follow the liver, lungs, spleen, central nervous system. The most resistant to the condition of pathogenic factors of muscle are connective and bone tissue.
Dystrophy
Dystrophy is a complex pathological process that occurs in the body due to metabolic disorders and manifested changes in the properties and morphology of cells and tissues, which leads to morphological changes in the body. Thus, dystrophy is the morphological equivalent of metabolic disorders. At the heart of dystrophy is enzymopathy, when metabolic processes, responding to the impact of the external or internal environment, quantitatively and/or qualitatively changed, which leads to a modification of cells and, consequently, tissues. Dystrophy can be in the cell itself, in the intercellular space, as well as in the cell, and in the intercellular space. Dystrophy can affect the entire body, or organ, or organ system, or even part of the body.
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Mechanisms of dystrophy development
Dystrophy develops through 4 mechanisms:
1.Pathological infiltration, that is, drift with blood flow of certain substances, followed by their accumulation in the tissue. For example, skidding of drops of fat.
2.Pathological transformation is the transformation of some substances into others, with the accumulation of the latter in the tissues. For example, the transformation of proteins, carbohydrates into fat and its accumulation in tissues.
3.Decomposition - destruction of the cytoplasmic complex. In this case, the individual components of the cytoplasm become visible.
4.Perverted synthesis is the synthesis of abnormal pathological substances. For example, the synthesis of abnormal amyloid protein in amyloidosis.
Feature: these processes can be combined, to be taken in any order, but one definitely takes precedence.
Classification of dystrophy
A.By localization: depending on the prevalence of morphological changes in the parenchyma, in the stroma or in the parenchyma and in the stroma, dystrophy can be:
1. Cellular (parenchymal)
2. Extracellular (stromal vascular)
3. Mixed
B.By the prevalence of violations of metabolism:
1.protein (dysproteinosis)
2.fat (lipids)
3.carbohydrate
4.mineral
C.Depending on the influence of genetic factors: 1. hereditary
2. acquired
D.By dissemination of the process:
1.general
2.local
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Violation of protein metabolism. Dysproteinosis.
Divided into:
1.Parenchymatous
2.Stromal vascular
3.Mixed
Parenchymal dysproteinosis
This protein dystrophies, which have a large variety of forms and relate to all the protein that is available in the cell. It is characterized by the formation of grains of protein nature, or vacuoles, which contain liquid with protein. The essence of parenchymal dysproteinoses: protein of cytoplasmic origin is chemically, physically and morphologically takes a different view, different from the norm. Often it either denatures, or liquefies. The mechanisms of development of such dystrophy may be pathological infiltration, perverted synthesis, decomposition.
This includes 4 types of dystrophy:
1.Granular (turbid swelling)
2.Hyaline droplet degeneration
3.Vacuolar (hydropic, balloon)
4.Keratinous
Granular degeneration or cloudy swelling
This is a mild form of parenchymatous dysprpteinosis, characterized by the appearance in the cytoplasm of cells small, dust-like granules and drops of protein nature.
Etiology: mild infectious diseases, intoxication, circulatory disturbances, etc. The important thing is that all of these reasons result in the development of hypoxia and accumulation of acidic products.
Pathogenesis: swelling and condensation of mitochondria, which dramatically increases the hygroscopicity of the cytoplasm of the cell, in consequence of which the cell swells morphologically, increases in volume, and its cytoplasm becomes heterogeneous, with dusty grain.
Pathology: most commonly affects the liver, kidneys, myocardium. Macro: organs are swollen, of flabby consistency, the capsule is tense, with the surface and on the cut on - painted whiter than usual, dull species, on the cut - parenchyma bulges, drawing authority from
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the surface and the cut - smoothed. Parenchyma can be penetrated by small-point hemorrhages.
Micro: affected cells are dramatically increased in volume, the cytoplasm is increased in volume, with a small presence when painting with hematoxylin-eosin of light pink dust grains. Some cells lose their nuclei.
Outcome and importance for the body: a mild form of dystrophy, after the termination of the influence of the pathogenic factor, the morphology of the body returns to normal. If the effect of the pathological factor persists-it goes into a more severe form of dystrophy.
Hyaline droplet degeneration
It is a severe form of parenchymal deproteinosis characterized by the presence in the cytoplasm of cells large, homogeneous half luminous drops of protein nature.
Etiology: acute and chronic infections, severe intoxication, poisoning, severe allergic reactions, severe inflammation.
Pathogenesis: this is the resorption of cytoplasmic proteins and their subsequent denaturation in the cytoplasm of cells.
Pathology: most commonly affects the liver, kidneys. Macro: almost not recognized.
Micro: in the cytoplasm of cells a huge number of large oxyphilic drops of protein nature accumulates (deep pink color when stained with hematoxylin-eosin). Many cells lose their nuclei.
Clinically, it is manifested by the insufficiency of the affected organ, morphologically characterized by cell death, the formation of coagulation (dry) necrosis, followed by sclerosis of the organ, i.e., the growth of connective tissue.
Vacuolar degeneration
Severe form of dystrophy, characterized by the formation of cells in the cytoplasm of vacuoles of various shapes with a transparent liquid, which is poor in protein.
Etiology: severe infections, infestations, intoxication, especially poisoning in kidney disease, as well as specific forms of damage, such as smallpox, foot and mouth disease, herpes.
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Pathogenesis: changes in colloidal osmotic pressure and increased permeability of cell membranes, resulting in fluid accumulation in the cell.
Pathomorphology: the most often liver, kidneys, skin, myocardium suffer
Macro: almost not recognized
Micro: depenRS on the stage of the process.
Morphogenesis: at the beginning cytoplasm of the damaged cells sometimes brightens. Then small vacuoles are formed, which merge with each other, forming larger ones, until one huge vacuole is formed in the cell-the balloon, which pushes the cytoplasm and nucleus to the periphery. As a result, the following is formed: the cytoplasm and the nucleus are pushed to the cell border with the formation of a ringshaped cell.
Outcome and importance for the body: this is a severe form of dystrophy, clinically manifested by the insufficiency of the affected organ or tissue, morphologically, at the site of the lesion, a collicative (wet) necrosis develops with the outcome in the sclerosis of the organ (i.e., the growth of connective tissue).
Feature: when stained with hematoxylin-eosin it can be confused with large-drip fat dystrophy, so a special color – Sudan III on fat. Vacuum dystrophy with this color will not be painted, and large-drip fat dystrophy will be yellow.
Keratinous dystrophy
It is characterized by the accumulation in the tissues of the horny substance – keratin. In some cases, the amount of keratin may decrease, or it is synthesized in the pathogenic form.
Etiology: hereditary or congenital pathology, mechanical injuries, severe inflammation of the mucous membranes, specific infectionsherpes, etc.
Pathogenesis: very different, but in the end in the tissue structures deposition of keratin is observed.
Pathomorphology: manifests itself in the form of:
1.Hyperkeratosis is the excessive formation of keratin. It is more often in the skin, the epidermis thickens and becomes horny-corn.
2.Hypokeratosis is a hereditary pathology characterized by a reduced deposition of keratin. It is morphologically characterized by
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changes in the state of the flat keratinizing epithelium, formation of wounds, skin abrasions, as well as an abundance of hemorrhages.
3.Parakeratosis is an excessive deposition of keratin with a violation of its quality, and keratin is deposited in unusual places. This is the mucous membrane of the gastrointestinal tract, the rumen in ruminants, in preputia, visible mucous membranes.
4.Ichthyosis is a congenital deformity, characterized by excessive keratinization of almost the entire skin. The skin is rough, scaly, animals die in the first days of life.
Outcome and importance for organism: depends on the type and severity of the lesion.
Stromal vascular deproteinosis
These are protein dystrophies, which relate to the connective tissue system. Their four species are:
1.Mucoid swelling
2.Fibrinoid swelling
3.Hyalinosis
4.Amyloidosis
The first three forms are successive stages of connective tissue disorganization.
Mucoid swelling
This is the stage of superficial disorganization of connective tissue, which is the mucoid edema of the main substance of connective tissue.
Etiology: these are the mild effects of the pathogenic factor. Mild inflammations, intoxication.
Pathogenesis: in the connective tissue hyaluronic acid and factors of permeability accumulate, i.e. chondroitinase acids. These substances contribute to an increase in the permeability of the walls of blood vessels, where plasma proteins impregnate the connective tissue. There is hydration of connective tissue and swelling.
Macro: not shown.
Micro: it is weakly expressed and characterized by the spread of moderate type of connective tissue fibers and signs of edema of the main substance, that is, it is slightly increased in volume and is colored with eosin lighter.
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Outcome and importance for organism: this is a mild form of stromal-vascular deproteinosis, upon termination of the pathological factor in the disruption signs disappear, when you continue to pass into fibrinoid swelling.
Fibrinoid swelling
This is the stage of deeper connective tissue disorganization. Etiology: medium and severe forms of inflammation, exposure to
mechanical factors, viral and bacterial infections.
Pathogenesis: there is swelling of collagen fibers, their subsequent disintegration and impregnation of these fragments with plasma proteinfibrin.
Macro: not typical.
Micro: heavy waving of collagen and elastic fibers, the formation of lumpy or homogeneous light pink mass necrosis in their place.
Outcome and importance for the body: either hyalinosis or fibrinoid necrosis develop.
Hyalinosis
It is a severe form of stromal-vascular deproteinosis, characterized by the formation of homogeneous translucent dense masses, resembling hyaline cartilage.
Etiology: the leading cause in the development of hyalinosis is hypoxia. Then there is the destruction of fibrous structures, increase of vascular tissue permeability, resulting in the formation of protein hyaline. The reasons may be:
1.Severe infections and intoxication
2.Severe inflammation
3.Deep disorders of local blood circulation
Hyaline is a fibrillar prote the base of which are fibrin, immunoglobulins and lipids. All this complex of substances under the influence of tissue enzymes is transformed into a new pathological protein hyaline.
Physical and chemical features of hyaline:
1.Uniformity and translucency
2.Eosinophilia
3.Resistance to acids, alkalis, enzymes
4.Positive reaction to polysaccharides
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Hyalinosis can be local and generalized.
Pathomorphology: hyalinosis of small arteries, arterioles is systemic in nature and is most pronounced in the kidneys, pancreas, gonads.
Macro: general hyalinosis is detected with difficulty. The vessels lose elasticity, become like glass tubes, the organ is pale, dense, dryish, reduced in volume, the pattern from the surface and on the section is smoothed.
Micro: hyaline accumulates in the vessel wall, making it homogeneous and sharply increased in volume. In this case, the vessel lumen sharply narrows, and the wall thickens at times. The so-called fabric coupling is formed.
Local hyalinosis is the outcome of sclerosis, that is, the growth of connective tissue. It is observed in scar tissue and in the tumor stroma. At the same time, microscopically uniformity of connective tissue is noted, cell structures disappear, fibers decrease sharply in number, their place is occupied by hyaline (when stained with eosin - pink).
The outcome and importance for organism: depends on the localization and distribution of process. Hyalinosis is irreversible.
Amyloidosis
This is a special vascular-stromal desproteidos, which consists in the synthesis and accumulation in the body of a particular pathogenic protein – amyloid.
Etiology: the causes of amyloidosis are severe purulent inflammation, the presence in the body of extensive necrotic processes, severe intoxication.
Pathogenesis: protein-amyloid is produced by abnormal cells - amyloidoblasts. The composition of this protein includes:
1. Fibrillar protein that is produced by amyloidblasts
2.Globular plasma protein
3.Glycopolysaccharides Features of amyloid:
1.Very resistant to acids, alkalis and enzymes and resists rot
2.Gives an intense coloration when exposed Lugol’s solution.
3.It is macroscopically homogeneous and semi-transparent The morphogenesis of amyloidosis includes 4 stages:
1.The appearance of amyloidoblasts
2.The synthesis of an abnormal fibrillar protein
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3.The formation of a fibrillar skeleton
4.Impregnation of the fibrillar frame with plasma proteins, fibrin and polysaccharides.
Feature: sources of amyloidoblasts are fibroblasts, reticular cells, plasma cells, lymphocytes.
Pathomorphology: in organs and tissues amyloid is deposited in two types:
1.Along the way of reticular fibers. Spleen, liver, kidneys, adrenal glands, intestines are affected.
2.Along the way of collagen fibers. This affects the large and medium arteries, heart, nerves, skeletal muscles, skin.
Amyloidosis can be general and local.
Pathomorphology of amyloidosis of the spleen
It exists in focal and diffuse form.
Focal form, or" sago spleen": amyloid masses are deposited exclusively in the white pulp, causing an increase in its volume and atrophy of the red pulp. On the surface of the body, the follicles of the white pulp are clearly revealed. This is very large, protruding on the general surface of the red pulp whitish grains that resemble sago grain.
Diffuse form of amyloidosis of the spleen ("greasy "or" ham spleen") is a continuation of the sagic form, in which the deposition of amyloid in both white and red pulp is noted, while the spleen is sharply increased in volume, its capsule is tense, it acquires a light pink color and resembles fat and ham in the section.
Pathomorphology of amyloidosis of the liver
Macro: the liver is enlarged in volume, light pink, the capsule is tense, the liver is brittle, easily torn by hands, the cut pattern of the body is blurred (the structure is not preserved).
Micro: depends on extent of injury. In severe and medium cases, there is a violation of histoarchitectonics, disturbed lobular structure of the liver, amyloid is deposited in the inter-girder space, which leads to atrophy of hepatocytes from pressure, their place is replaced by amyloid.
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