100. Dysplasia (intraepithelial neoplasia) of the epithelium as a precancerous process: definition of the concept, types, causes, significance for the body, examples.

Dysplasia is a pronounced violation of the proliferation and differentiation of the epithelium with the development of cellular atypia and a violation of histoarchytictonics.

Cellular atypia is represented by various cell sizes and shapes, an increase in the size of nuclei, hyperchromia, and the appearance of atypical mitoses.

Violation of histoarchytictonics is a loss of epithelial polarity, but the basement membrane is not broken.

3 stages of dysplasia in accordance with the degree of proliferation and severity of cl. and tissue atypia.

1)light(small) } reversible

2)moderate(medium) }

3) severe (significant) - precancerous

Dysplasia occurs mainly in inflammatory and regenerative processes, reflecting a violation of cell proliferation and differentiation. Its initial stages (I-II) are difficult to distinguish from pathological regeneration, especially considering that dysplasia and metaplastic epithelium may occur. These stages of dysplasia are most often reversible. Changes in severe dysplasia (stage III) are much less likely to reverse development and are considered precancerous - precancerous. Sometimes they are difficult to distinguish from carcinoma in situ ("cancer in situ").

The term dysplasia is used in relation to a wide variety of diseases, which are based on an abnormality in the development of a tissue, cell or organ:

• Hip dysplasia,

• Connective tissue dysplasia,

• Fibrous dysplasia,

• Metaepiphyseal dysplasia,

• Cervical dysplasia.

The term "dysplastic" is applied to any pathological process, the etiology of which is dysplasia:

• Dysplastic coxarthrosis,

• Dysplastic status,

• Dysplastic scoliosis.

101. Definition of the concept and basic properties of the tumor. The difference between tumor growth and tissue growth during regeneration, hyperplasia, chronic inflammation.

A tumor, neoplasm, blastoma is a pathological process characterized by unrestrained cell proliferation, while violations of cell growth and differentiation are caused by changes in their genetic apparatus.

The main properties of the tumor are autonomous and uncontrolled growth, the presence of atypism, the ability to progress and metastasis.

Autonomous tumor growth.

It is characterized by a lack of control over cell proliferation and differentiation on the part of the tumor-bearing organism and is expressed in the loss of contact inhibition and immortalization (acquisition of immortality) of tumor cells.

In malignant tumors, autonomous growth is expressed to a large extent, and they grow rapidly, germinating the surrounding normal tissues. In benign tumors, autonomous growth is poorly expressed.

Tumor atypism.

There are 4 types of atypism in tumors:morphological, biochemical, antigenic and functional.

Morphological atypism is represented by two variants: tissue and cellular. Tissue atypism is expressed in a change in the relationship between the parenchyma and the tumor stroma, more often with a predominance of parenchyma; a change in the size and shape of tissue structures with the appearance of ugly tissue formations of various sizes. Cellular atypism consists in the appearance of cell polymorphism both in shape and size, enlargement of nuclei in cells with often indented contours, an increase in the nuclear-cytoplasmic ratio in favor of the nucleus, the appearance of large nucleoli and intracellular inclusions. As a result of pathological mitoses, hyperchromic nuclei are found in tumor cells, and multinucleated cells are formed.

Malignant tumors are characterized by both types of morphological atypism. Benign tumors are characterized only by tissue atypism, since they are built from mature, differentiated cellular elements.

Biochemical atypism. It manifests itself in metabolic changes in tumor tissue. All metabolic rearrangements in the tumor are aimed at ensuring its growth and adaptation to the relative oxygen deficiency that occurs with rapid tumor growth. Enhanced synthesis of cancer proteins, growth factors and their receptors, a decrease in the synthesis and content of histones, the synthesis of embryonic proteins and receptors for them, the transformation of tumor cells into facultative anaerobes, and a decrease in cAMP content are recorded in tumor cells. Biochemical atypism can be studied using morphological methods — histochemical and immunohistochemical, therefore it is also called histochemical atypism.

Antigenic atypism of tumors manifests itself in the formation of tumor-specific antigens, oncophetal antigens, as well as in the loss of histocompatibility antigens, tissue-specific antigens by some tumors, which leads to the development of antigen-negative tumors and the formation of tolerance to them.

Functional atypism. It is characterized by the loss of tumor cells of specialized functions inherent in similar mature cells, and / or the appearance of a new function that is not characteristic of cells of this type. For example, cells of low-grade scyrrhous cancer stop producing secretions and begin to intensively synthesize collagen of the tumor stroma.

The ability to progress is a change in the totality of tumor signs (genotype, karyotype and phenotype of tumor cells, including various features of their morphological, biochemical or other differentiation) in the direction of an increasing increase in malignancy.

The increase in malignancy is associated with the consistent appearance of cellular subpopulations with geno- and phenotypic differences from their predecessors, which are represented by such properties and signs as invasiveness, a change in growth rate, the ability to metastasize, the appearance of a new karyotype, other sensitivity to hormones and antitumor drugs. Therefore, despite the fact that initially most malignant neoplasms have a monoclonal origin, by the time of their clinical detection, the cells that make up their parenchyma are characterized by pronounced heterogeneity in geno- and phenotypic terms.

TUMOR GROWTH

Depending on the degree of differentiation, there are three types of tumor growth: expansive, appositional, infiltrating (invasive).

With expansive growth, the tumor grows out of itself, pushing aside the surrounding tissues. Parenchymal elements of the tissue surrounding the tumor atrophy, stroma collapse develops, and the tumor becomes surrounded by a capsule (pseudocapsule).

The expansive growth of the tumor is slow, typical for mature, benign tumors. However, some malignant tumors (kidney cancer, thyroid cancer, fibrosarcoma) can also grow expansively.

The appositional growth of the tumor occurs due to the neoplastic transformation of normal cells into tumor cells that are located in the tumor field.

With infiltrating (invasive) growth, tumor cells grow into the surrounding tissues and destroy them (destructive growth). Invasion usually occurs in the direction of least resistance along the interstitial tissues, along the course of nerve fibers, blood and lymph vessels. Tumor cell complexes destroy the walls of blood vessels, penetrate into the blood and lymph flow, grow into loose connective tissue. If an organ capsule, membrane and other dense tissues are found along the path of tumor invasion, tumor cells first spread along their surface, and then, germinating the capsule and membranes, penetrate into the depths of the organ. The boundaries of the tumor with its infiltrating growth are not clearly defined. Infiltrating tumor growth is rapid, characteristic of immature, malignant tumors.

In relation to the lumen of the hollow organ, tumor growth can be endophytic or exophytic. Endophytic growth is the infiltrating growth of a tumor deep into the wall of an organ. In this case, the tumor from the mucous membrane (for example, stomach, bladder, bronchus, intestines) is almost invisible; on the section of the wall it is visible that a tumor is germinating. Exophytic growth is the expansive growth of a tumor into the cavity of an organ (for example, stomach, bladder, bronchus, intestines). In this case, the tumor can fill a significant part of the cavity, connecting to the wall with its leg.

Depending on the number of foci of the tumor, they talk about unicentric (one focus) and multicentric (multiple foci) growth.

102. Tumors: definition of the concept, theory of occurrence. Signs of cellular and tissue atypia in tumors.

A tumor, neoplasm, blastoma is a pathological process characterized by unrestrained cell proliferation, while violations of cell growth and differentiation are caused by changes in their genetic apparatus.

1) Physico-chemical theory reduces the occurrence of tumors to the effects of various physical factors (temperature, ionizing radiation) and chemical, so-called carcinogenic substances (coal tar, 3, 4 - benzpyrene contained in tobacco smoke).

2) Viral and viral genetic theory assigns a crucial role to oncogenic viruses in the development of tumors.

3) Dysontogenetic theory suggests that a number of tumors arise as a result of dislocations and vicious development of tissues of embryonic leaves.

4) The political etiological theory combines the above-mentioned causes as possible in the formation of tumors.

Tissue atypism is expressed in a change in the relationship between the parenchyma and the tumor stroma, more often with a predominance of parenchyma; a change in the size and shape of tissue structures with the appearance of ugly tissue formations of various sizes. Cellular atypism consists in the appearance of cell polymorphism both in shape and size, enlargement of nuclei in cells with often indented contours, an increase in the nuclear-cytoplasmic ratio in favor of the nucleus, the appearance of large nucleoli and intracellular inclusions. As a result of pathological mitoses, hyperchromic nuclei are found in tumor cells, and multinucleated cells are formed.