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

The secondary ones are acquired and morphologically manifest by the involution of the organs, and most importantly, microscopically: the desolation of the organs of the immunocompetent system. That is, in the lymphoid tissue there are extensive fields with a small number of immunocompetent cells, or they do not exist.

Adaptive and compensatory reactions

Under the action of pathological factors, the body responds to them either by adaptation reactions or compensation reactions. Adaptive reactions occur when the tissue is not damaged, but only adapts to changing environmental conditions. Compensation reactions occur when it is necessary to fill the existing defect that has arisen under the influence of pathological factors.

Adaptive reactions include:

1.Atrophy

2.Hypertrophy and hyperplasia

3.Organization

4.The restructuring of the tissue

5.Metaplasia

6.Dysplasia

Compensatory reactions include:

1.Regeneration

2.Hypertrophy

3.Hyperplasia

4.Healing

Differences of adaptive reactions from compensatory:

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Hypertrophy and hyperplasia

Hypertrophy is an increase in the volume of organs due to an increase in the volume of cells without increasing their number.

Hyperplasia – an increase in the volume of the body due to the reproduction of cells.

In structural (morphological) relation these processes are similar. So I say hypertrophy, and hyperplasia mean.

Hypertrophy can be true and false.

True hypertrophy is an increase in the volume or quantity of all tissue elements in all tissues that make up the organ (i.e. both parenchyma and stroma). This pathological process is proportional both in the parenchyma and in the stroma.

Signs: the increase in volume and mass of the body. The edges of the organ are thickened, they become cylindrical, the number of parenchymatous elements increase, there is an intense painting of the body. The most important feature is the preservation of the usual form of the organ and the proportionality of tissues.

False hypertrophy is an increase in the volume and mass of the organ, but due to the difference in the content of water or fat tissue in it.

Morphological features: the increase in the volume of the organ, the number of parenchymal elements is reduced. In the organ connective or fatty tissue grow, so the shape of the it changes, it becomes less fullblooded, its color brightens. The functions of the organ are reduced, the process is irreversible.

By the significance hypertrophy can be pathological and physiological.

Physiological hypertrophy is an increase in the volume and mass of the organ due to its functions under the influence of natural causes (adequate stimuli). For example, hypertrophy of the uterus during pregnancy, hypertrophy of the breast during lactation. Feature: reversibility.

Pathological hypertrophy is an increase in the volume of organs as a result of exposure to extraordinary stimuli.

It may be:

1. Working (compensatory). It is observed under excessive load (hypertrophy of the digestive tract in the presence of obstacles).

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2.Vicar (replacement) hypertrophy. There is a removal, necrosis of one of the paired organs or part of the unpaired. In this case, the remaining organ assumes the functions of the damaged.

3.Neurohumoral hypertrophy. It is observed in connection with the new impact of the nervous or humoral system. Hypertrophic growth leads to an increase in the size of tissues, organs, which occurs as a result of the growth of connective tissue (elephant, wild meat).

Metaplasia

Metaplasia (from lat. "metaplaco" – "to turn") is a transition from one tissue to another, related source. Metaplasia always occurs in connection with the proliferation of undifferentiated cells. Most often metaplasia is exposed to the epithelium. For example, the conversion of glandular epithelium into intestinal epithelium or metaplasia of the prismatic epithelium into flat keratinizing epithelium. Metaplasia of connective tissue leads to its transformation into cartilage or bone. Myeloid metaplasia is known – it is the transformation of one myeloid tissue to another (in the spleen and lymph nodes).

The restructuring of tissues is observed in any tissue with a change in its load. For example, collateral circulation, bone restructuring with changes in stress, load on it, adaptive changes (histological accommodation).

Dysplasia

This is a violation of the proliferation and differentiation of the epithelium with the development of cell atypia and histoarchitecture.

Features: dysplasia is of the tissue, not cellular.

There are 3 degrees of dysplasia: light, moderate and heavy.

Regeneration (regenerative reactions)

This is the restoration or replacement of structural elements of tissues instead of lost or dead. Regeneration can take place at various levels: molecular, ultrastructural, cellular, tissue, organ. The degree of development of regeneration and restoration of structures depends on the level of tissue organization. When regeneration is always a question of performing a strictly specialized function of regeneration (restoration of structures with the restoration of the organ function), that is,

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regeneration is involved in the process of material support of homeostasis.

Restoration of structure and function are possible with the help of cellular and intracellular hyperplastic processes, so there are two morphological forms of regeneration:

1.Cellular: it is cell proliferation and mitotic and amytic way. In this case, the fabric is restored almost completely.

2.Intracellular: it develops due to the increase in the number (hyperplasia) and size (hypertrophy) of ultrastructural cell components. Feature: intracellular regeneration is universal. It is intrinsic to all organs and tissues.

In some organs and tissues there is a cellular and intracellular form of regeneration, that is, mixed regeneration.

To organs and tissues, which are dominated by cellular form of regeneration, epithelial, bone, loose connective, hematopoietic refer to. To the organs and tissues of the hybrid include regeneration of the glands (liver, pancreas, and kidneys). Organs and tissues with intracellular regeneration include myocardium, skeletal muscle, central nervous system.

Feature: in the central nervous system intracellular form of regeneration is the only form of regeneration, and mytochondria are very poorly subjected to the regeneration.

From a biological point of view, there are three types of regeneration:

1.Physiological: occurs continuously throughout life. Renewal of cells, fibrous structures, epithelium, hair.

2.Reparative: it develops in various pathological processes, which are accompanied by tissue alteration.

3.Pathological: develops in a number of special reasons, when the regenerative process is perverted and manifests itself in the form of excessive appearance or insufficient formation of tissues.

The mechanism of reparative and physiological regeneration is the same. Reparative regeneration-enhanced and modified physiological regeneration. Reparative is induced by pathological processes and can be complete and incomplete.

Full reparative regeneration is a full compensation of the defect with an identical tissue. It is observed in tissues with cellular form of regeneration.

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Incomplete reparative regeneration is characterized by the replacement of the defect with connective, scar tissue. It is observed in organs and tissues, where intracellular regeneration prevails.

Organization and healing of wounds

Organization - is the replacement of the area of tissue defect (necrosis, blood clot, etc.) connective tissue. Typical examples: healing of wounds, the organization of thrombus.

Wound healing can go in four ways:

1.Closure of the defect with the epithelium. The simplest form of wound healing, is observed in damage to the epidermis, especially the linear nature (scratches). Occurs through layers of the epithelial tissue on the defect with overlap of the defect.

2.Wound healing under the scab. At a superficial and imposed wound. Most often it is damage to the papillary layer of the skin, where the vessels pass. On the surface of the wound the blood and lymph go out that dry to a crust (scab). Under the scab, the reproduction of the epidermis is activated, which closes the defect. After 5-7 days, the scab disappears and the wound heals.

3.Wound healing by primary intention. The wound should be: with a flat surface, little seeded, the edges of the wound close to each other, the wound should be shallow. Mechanism of healing: the wound edges swell and become bloodshot, they rise, beneath the surface of the fabric, infiltrate by phagocytes, which phagocyte dead substrate. In 2-3 days, a special connective tissue rich in vessels (granulation) is formed. This is a kind of temporary organ that creates the body in pathological conditions for the implementation of protective (barrier) reparative function. Granulative tissue activates the reproduction of fibroblasts (protein biosynthesis and fibrillogenesis). The interaction of fibers with fibroblasts expands the vessels of MCR and, eventually, forms a mature connective tissue, which is flooded with epithelium and in 7-10 days there is a complete closure of the defect – skin scar.

4.Wound healing by secondary intention. Reaction in conditions of large and deep open defect, with microbial contamination and abundance of dead substrate. Is formed around the powered zone of demarcation of inflammation. On 5-6 day the exclusion of the dead masses happens, cleansing of the wound by phagocytes takes place, then granulation tissue forms. Gradually the granulation tissue fills the

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defect. As a result, the granulation tissue turns into a mature coarse fibrous connective tissue, which is impregnated with plasmocytes, is subjected to hyalinosis, and turns into a coarse fibrous scar, which remains visible for many years.

Tumor growth

Tumor (neoplasm, blastoma) - a kind of tissue growth, which differs from other forms of growth, uncontrolled autonomous growth, by poorly differentiated structure of mature atypical cells.

Etiology. Each cell of the body has cellular oncogenes and antioncogenes. Cellular oncogene – DNA region which is homologous to viral oncogenes. In the active state such areas are called cell oncogenes. In the inactive – proto-oncogenes – these are normal genes cells. In mature tissues, they are inactive. Activation and transformation of cellular oncogenes occurs during tumor growth, as well as during embryogenesis. Under the action of pathogenic factors of external environment, mutagenic factors, proto-oncogenes are activated and begin to produce specific proteins oncoprotein. 80% of all oncoproteins are growth factors, 20% oncoproteins (oncoproteins) – receptors for growth factors of the body. Thus, changing, the cell mutates and turns into a precancerous cell that processes cancer cells, contributing to the maintenance of its development and unlimited reproduction. That is, the cancer cell acquires immortalization (immortality).

The pathogenesis of malignant tumors passes in 4 stages:

1.Changes in the genome of a somatic cell under the influence of various carcinogenic agents, often in the presence of hereditary changes.

2.Activation of cellular oncogenes and suppression of antioncogenes.

3.Expression of cellular oncogenes, disruption of regulatory gene production.

4.Malignant transformation of cells with the acquisition of the ability to autonomic growth.

The main properties of the tumor

Depending on the stage of maturity, growth rates, the nature of growth, the ability to metastasize and relapse, benign and malignant tumors are distinguished.

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Benign tumor: built of mature, differentiated cells, has a slow expansive growth with the formation of a capsule of connective tissue on the border with the surrounding normal tissue (tumor growth in itself). The tumor does not recur, does not metastasize. The name of a benign tumor is formed based on the name of the original tissue and the ending “Om” (fibroma, lipoma).

Malignant tumor: built of partially or completely undifferentiated cells. Grow rapidly, the surrounding tissues (infiltrating growth) sprout, tissue structures (invasive growth) sprout, can recur and metastasize. Malignant tumors of the epithelium are called cancer or carcinoma. Tumors of the mesenchymal, i.e. connective tissue, are called sarcoma.

The main features of tumors:

1.Autonomous growth

2.The presence of atypical

3.Ability to progress and metastasize

Autonomous growth of tumors is characterized by the lack of control over the proliferation and differentiation of cells from the tumor-bearing organism. In this case, the tumor cells pass to the autocrine and paracrine mechanisms of growth regulation. In autocrine stimulation, tumor cells produce growth factors or analogues of growth factors, or receptors to growth factors. Autonomous tumor growth is expressed in the loss of contact inhibition and immortalization (i.e. the acquisition of immortality by the tumor cell). Autonomy is relative. The tumor constantly receives nutrients, hormones, oxygen, cytokines from the body. That is, autonomy is not complete independence, but the acquisition of the tumor's ability to self-government. In malignant tumors, autonomous growth is very pronounced. They grow quickly, sprouting in the surrounding tissue. In benign tumors, autonomous growth is very weak. They grow slowly and do not germinate in the surrounding tissue.

Tumor atypism is a deviation from the norm. In addition, the tumor is characterized by anaplasia (return to the embryonic stage of development), cataplasia (likening of embryonic tissue).

The tumors secrete 4 types of irregularities:

1. Morphological atypism: tumor tissue does not replicate the structure of mature tissue, and tumor cells may not be similar to mature cells of the same origin. Morphological irregularities are presented by tissue and cell irregularities. Tissue atypism is a change in the ratio

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between parenchyma and tumor stroma, most often with a predominance of parenchyma. Cell atypism-polymorphism of cells in form and size. The cells become larger in nucleus, nucleus change their form, altered nuclear-cytoplasmic ratio, nucleoli appear temporary, the figures of division. In tumor cells as a result of mitosis cells with hyperchromic nuclei form. Malignant tumors are inherent in both types of morphological atypism. Benign tumors are characterized only by tissue atypism, because they are built of mature differentiated cells.

2.Biochemical atypism: in metabolic processes in tumor tissue. In this case, in the tumor cells , enhanced synthesis of cancer cells, growth factors and the transformation of tumor cells into facultative anaerobes are recorded. At the same time, the tumor is experiencing a constant lack of oxygen and nutrients.

3.Antigenic atypism. There are 5 types of antigens in tumors:

1.Antigens of viral tumors

2.Caused by carcinogens

3.Tumour-specific

4.Embryonic

5.Heterogeneous

Antigenic atypism manifests itself in the formation of tumor-specific antigens, as well as in the loss of some tumors histocompatibility, which leads to the formation of immunological tolerance towards tumors.

4. Functional atypism: characterized by the loss of tumor cells of specialized functions, similar to other cells, or the appearance of a new function, not peculiar to this type of cells.

The progression of the tumor is an increase in the volume of the tumor, which is determined by its autonomy and the production of BAS. With an increase in malignant tumor progression occurs in the direction of increasing malignancy, one of the manifestations of which is the development of metastases.

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Bibliography

1.Акулов А.В., Пичугин Л.М. Практикум по патологической анатомии сельскохозяйственных животных. 2-е изд., испр. и доп. – М.: Колос, 1980.

–288 с.

2.Атлас-альбом / под ред. проф. Б.Л. Белкина, А.В. Жарова. – М.: Аквариум Принт, 2013. – 232 с.

3.Бажибина Е.Б., Ватников Ю.А. Особенности структуры почек в условиях острой гиповолемии при спонтанной множественной травме // Российский ветеринарный журнал. Мелкие домашние и дикие животные. - 2008. - № 1. - С. 16-20.

4.Бинхун Х., Ватников Ю.А., Куликов Е.В., Попова И.А., Петрухина О.А. Лечение гнойного эндометрита у собак // Теоретические и прикладные проблемы агропромышленного комплекса. - 2018. - № 2 (35). - С. 27-31

5.Боли Б.И., Куликов Е.В., Ветошкина Г.А. Особенности топографии поджелудочной железы собак // Морфология. - 2018. - Т. 153. - № 3. - С. 46-47.

6.Боль Б.К. Патологоанатомическое вскрытие сельскохозяйственных животных (с патологоанатомической диагностикой инфекционных заболеваний). 4-е изд., перераб. и доп. – М.: Сельхозгиз, 1953. – 335 с.

7.Боль К.Г., Боль Б.К. Основы патологической анатомии сельскохозяйственных животных. – М.: Сельхозгиз, 1961. – 571 с.

8.Ватников Ю.А. Морфофункциональный анализ регионарных лимфатических узлов в процессе репаративного остеогенеза у лабораторных животных // Вестник Саратовского госагроуниверситета им. Н.И. Вавилова. - 2010. - № 3. - С. 7-9.

9.Ватников Ю.А., Куликов Е.В., Попова И.А., Сахно Н.В., Петряева А.В., Лыхина В.С., Газин А.А. Изменение клинических и биохимических показателей крови при хроническом гепатите у собак // Вестник Красноярского государственного аграрного университета. - 2018. - № 2 (137). - С. 62-69.

10.Ватников Ю.А., Куликов Е.В., Селезнев С.Б. Структурные изменения тимуса в период травматической болезни в условиях эксперимента // Российский ветеринарный журнал. Мелкие домашние и дикие животные. - 2010. - № 1. - С. 10-13.

11.Ватников Ю.А., Медведев И.Н., Боженова Е.Ю., Голева А.А.,

Сахно Н.В. Методы коррекции послеоперационного состояния собак при завороте желудка // Курск, 2017.

12.Ватников Ю.А., Родионов В.Д. Основы морфологии печени / В сборнике: Достижения современной науки Материалы Международной научно-практической конференции. - 2017. - С. 48-51.

79

13.Вскрытие животных и патологоанатомические диагнозы болезней / М.С. Жаков, В.С. Прудников, И.А. Анисим, В.В. Ванге-ев, В.М. Жаков. – Мн.: Ураджай, 1992. – 136 с.

14.Добин М.А., Кокуричев П.И. Практикум по ветеринарной патологической анатомии и вскрытию. 2-е изд., перераб. и доп. – Л.: Колос (Ленингр. отд-ние), 1975. – 295 с.

15.Есина Д.И., Селезнев С.Б., Куликов Е.В. Ультразвуковая диагностика поджелудочной железы собак // Инновационные про-цессы в АПК: сб. статей. – М.: РУДН, 2014. – С. 186-188.

16.Жаров А.В. Патологическая анатомия животных. 2-е изд., перераб.

идоп. – СПб.: Лань, 2013. – 608 с.

17.Жаров А.В. Практикум по патологической анатомии сельскохозяйственных животных / А.В. Жаров, И.В. Иванов, А.А. Кунаков и др. – М.: Агропромиздат, 1989. – 288 с.

18.Журавлева Л.Д. Структура патологоанатомического ди-агноза и клинико-анатомического эпикриза. – Ульяновск: УГСХА, 2007. – 22 с.

19.Инатуллаева Л.Б., Ватников Ю.А., Вилковыский И.Ф., Воронина Ю.Ю. Гистологические изменения в почках при хронической болезни почек у кошек, связанные с отложением амилоида // Ветеринария, зоотехния и биотехнология. - 2017. - № 5. - С. 25-31.

20.Инатуллаева Л.Б., Ватников Ю.А., Сахно Н.В. Фиброз почек при хронической почечной недостаточности III стадии у кошек // Russian Journal of Agricultural and Socio-Economic Sciences. 2017. - № 7 (67). - С. 298-303.

21.Кротова Е.А., Селезнев С.Б., Куликов Е.В. Морфологические аспекты иммунной системы кур при аэрозольной вакцинации // Морфология .- 2018. - Т. 153. - № 3. - С. 153-153a.

22.Куликов Е.В., Боли Б.И., Селезнев С.Б. Патоморфологические изменения при панкреатите у собак // Морфология. - 2018. - Т. 153. - № 3. - С. 159.

23.Куликов Е.В., Ватников Ю.А., Альбикова Г.М. Общая гистология с основами цитологии и эмбриологии. – М.: РУДН. 2012. – 188 с.

24.Куликов Е.В., Ватников Ю.А., Сачивкина Н.П. Частная патологическая анатомия. – М.: РУДН. 2013. – 76 с.

25.Куликов Е.В., Ветошкина Г.А., Рысцова Е.О. Морфологические особенности костного мозга у цесарок // Морфология. - 2016. - Т. 149. - № 3. - С. 117.

26.Куликов Е.В. Патологоанатомическая практика и верификация патогистологического диагноза: учеб. пособие / Е.В. Куликов, В.И. Паршина, Ю.А. Ватников. – М.: РУДН, 2017. – 188 с.: ил.

27.Куликов Е.В., Селезнев С.Б., Ветошкина Г.А. Морфологические показатели костного мозга у цесарок белой волжской породы // Морфология. - 2014. - Т. 145. - № 3. - С. 109-109aa.

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