Animal anatomy, histology, pathological anatomy

BIBLIOGRAPHY
1. Zharov A.V. Pathological anatomy of animals. – St. Petersburg; M.; Krasnodar: Lan, 2013. – 620 p. – Access mode: EBS “Lan” (http://e.lanbook.com), ISBN: 978-5-8114-1450-5 2. Zharov A.V. Forensic veterinary medicine.

Topic 4: Pathomorphology of inflammation and tumors

Plan
1. Etiology, pathogenesis and morphological signs of inflammation.
2. Types of inflammation depending on the composition of the exudate.
3. Etiology, pathogenesis and morphological features of tumors.


Keywords: tumors, leukemia, atypism, immature, histogenetic, metastasize, leiomyoma, adenoma, carcinoma, cancer,sarcoma, expansive, infiltrative,inflammation, diffuse.
1. Inflammation is characterized by change, exudation and proliferation. Change signifies damage and is characterized by atrophy, degeneration and necrosis.
On the other hand, exudation is characterized by hyperimmune exudation and emigration. Proleferatsiya cell reproduction and tissue repair The pathogenesis of any type of inflammation begins with damage to tissues and cells. In the affected tissues, metabolism is disrupted and dystrophic changes develop, atrophy of cells and tissues develops, cell destruction is characterized by necrosis, vascular permeability in the affected tissue. The formation and formation of exudate is characterized by emigration of formed elements and the formation of exudates of different compositions.
Causes. Exogenous or endogenous factors included. Exogenous causes are physical, chemical, mechanical and biological factors.
Foci of necrosis and salt deposits, etc., form in endogenous tissues.
Pathomorphology Macroscopic view. The size of the inflamed organs increases, the consistency can be hard or soft, dense, and the color changes depending on the composition of the exudate; exudate appears on the cut surface. Microscopic view. In histological preparations we see the composition of the exudate and changes in tissue cells under the influence of the exudate.
Exudative inflammation is very common. The fluid formed as a result of the leakage of a blood component from the vessel wall is called exudate.
2. The next exudative inflammation occurs in serous, hemorrhagic, fibrinous, purulent catarrhal inflammation.
Serous inflammation. Inflammation caused by the leakage of a portion of blood serum from the vessel wall. This inflammation is the initial stage of any complex inflammation and is characterized by the formation of exudates rich in simple proteins, albumin and globulins.
Hemorrhagic inflammation is characterized by the formation of exudate from the walls of blood vessels due to increased emigration of red blood cells; this inflammation is more common in infectious, predominantly viral diseases.
Fibrinous inflammation is characterized by the leakage of fibrinogen proteins from the vascular wall into the bloodstream and the formation of fibrin fibers as a result of its coagulation. This inflammation occurs in patients with pastrellosis.
Purulent inflammation is characterized by the formation of leukocyte-rich exudate as a result of the emigration of leukocytes from the walls of blood vessels. This inflammation occurs in septic diseases, anthrax, salmonellosis and others.
Catarrh. This inflammation occurs only on the mucous membranes and is characterized by the formation of a large amount of mucous substances as a result of hypersecretion of epithelial cells. This inflammation occurs with stomatitis, endometritis, mastitis and other diseases.
Modern teaching about inflammation and the macrophage system Inflammation is a complex protective-adaptive vascular-mesenchymal reaction of the body to tissue damage by various pathogenic factors. It is aimed at destroying the agent that caused the damage and restoring the damaged tissue. The inflammatory reaction develops in the territory of histion - tissues and cells in the area of ​​the microvasculature, which unites arterioles, precapillaries (precapillary arterioles), capillaries, postcapillaries (postcapillary venules) and venules. Inflammation consists of 3 sequentially developing phases: alteration, exudation and proliferation. The starting phase of inflammation - alteration is manifested by degeneration and necrosis of tissues and cells in the histion territory. In this case, inflammatory mediators of plasma and cellular origin are released (histamine, serotonin, leukokines, lymphokines, monokines, etc.). Particularly active mediators of inflammation are platelets, basophils, mast cells, neutrophils, lymphocytes and monocytes (macrophages). Inflammatory mediators stimulate the development of the second phase - exudation, which occurs in 6 stages: 1) inflammatory hyperemia of the blood vessels of the microvasculature; 2) increasing the permeability of the vascular wall; 3) exudation (exit from the lumen of the vessel) of the components of blood plasma; 4) emigration of blood cells; 5) phagocytosis; 6) formation of exudate and inflammatory cell infiltrate. The final phase of inflammation - proliferation (reproduction) ensures the restoration of damaged tissue or the formation of a scar. Thus, in phases 2 and 3 of inflammation, a cellular infiltrate and proliferation is formed from cells of hematogenous and histiogenic (local tissue) origin. Hematogenous cells at the site of inflammation include platelets, erythrocytes, neutrophils, eosinophils, basophils, T- and B-lymphocytes, plasmacytes (derivatives of Blymphocytes) and macrophages (MPF) - derivatives of blood monocytes. The cells of the SMF (macrophage system) include: blood monocytes, connective tissue histiocytes, Kupffer stellate cells in the liver, alveolar macrophages of the lungs, free and fixed macrophages of the lymph nodes, spleen and red bone marrow, pleural and peritoneal macrophages of the serous cavities, macrophages of the synovial membranes of the joints, osteoclasts of bone tissue, microglial cells of the nervous system, epithelioid and giant cells of infectious and invasive granulomas and foreign body granulomas. The main function of microphages (neutrophils and eosinophils) and macrophages (SMF) is phagocytosis of pathogenic agents of exogenous and endogenous origin. In addition, cells of hematogenous origin secrete inflammatory mediators that excite and support the inflammatory response, immunoglobulins (plasmocytes), and also perform regulatory and killer functions (Tlymphocytes). 20 The group of histiogenic cells includes cambial epithelial cells of the mucous membranes, skin, glands, and parenchymal organs; mast cells (tissue basophils, mast cells) and cells of the RES proper - adventitial and endothelial cells of blood vessels of the microvasculature, fibroblasts, fibrocytes and reticular cells. In the focus of inflammation, due to the proliferation of cambial epithelial cells, the parenchyma of an organ or tissue is restored; mast cells, like hematogenous cells, secrete inflammatory mediators; adventitial cells differentiate into fibroblasts and fibrocytes, which synthesize the ground substance, elastic and collagen fibers of connective tissue. Endothelial cells participate in the regeneration of blood vessels of the microvasculature; reticular cells synthesize reticular (argyrophilic) fibers and restore the reticular stroma of the immune system organs. Thus, the damaged parenchyma of organs and tissues in the inflammatory focus is restored by cambial epithelial cells. The function of the RES is to restore the connective tissue and reticular stroma of organs and tissues, as well as the regeneration of blood vessels of the microvasculature. 4.2. Phases of inflammation: alteration, exudation and proliferation, their relationship and interdependence Inflammation is a complex of tissue and vascular processes. These include: alteration, that is, tissue damage, exudation, which combines a complex of vascular-tissue changes, expressed in a violation of the permeability of the vascular wall with the release of blood elements and exudate beyond the wall, and proliferation - the reproduction of local tissue elements. The trigger for the onset of the inflammatory process is alteration; damage is followed by the phenomena of exudation and proliferation. Alteration, that is, tissue damage, can be expressed to varying degrees. Morphologically, alteration represents dystrophies of all types and necrosis. The mucous glands, under the influence of an irritant, begin to intensively secrete mucus, to which desquamated epithelium is mixed, and therefore the mucous membranes, when inflamed, are covered with a large amount of mucus, sometimes mixed with pus. Alteration determines the factor of tissue damage, and if these processes occur without hyperemia, exudation and proliferation phenomena, then they do not relate to inflammation. In the absence of one of the components of the inflammatory process, we cannot attribute it to inflammation. Exudation is a vascular reaction that occurs when tissue is damaged. The disorder is accompanied by an increase in vascular-tissue permeability and the release of exudate and cellular blood elements from the lumen of blood vessels into the perivascular space. Disruption of blood and lymph circulation is one of the most striking morphological signs of inflammation. The change in blood vessels begins with a reflex contraction of the lumen of small arteries and arterioles, capillaries, which is subsequently replaced by the expansion of the entire vascular zone at the site of inflammation. With inflammation of the lymphatic vessels, lymph flow first accelerates and then slows down, in this case, the lymphatic vessels become overfilled with lymph and leukocytes. Sometimes lymphothrombosis occurs in them. When examining tissue from the inflamed area under an electron microscope, emigration of leukocytes is noted, which occurs between the endothelial cells of the capillaries. The majority of leukocytes migrating through the vessel walls are neutrophilic leukocytes. Exudates differ not only in protein content, but also in cellular composition. In some cases, neutrophil cells predominate, in others - mononuclear cells (monocytes) and others; in addition, cells are attached that are rejected from the mucous membranes and other integuments. The main cellular elements involved in proliferation processes are local RES cells. These include reticular cells, histiocytes, epithelioid, lymphoid, plasma cells, mast fibroblasts, fibrocytes and all mesenchymal cells classified as connective tissue. These cells multiply, increase in number and make up the bulk of cellular elements during inflammation. 4.3. Nomenclature of inflammation The name of inflammation is determined by the Greek, less often Latin, name of the affected organ and the ending it (Latin itis). For example: bronchitis, splenitis, gastritis. There are exceptions to this rule. For example - pneumonia. Inflammation of the lining or capsule of an organ is denoted by the prefix peri (Greek about): pericarditis - inflammation of the outer lining of the heart, perihepatitis - inflammation of the liver capsule. When there is inflammation of the connective tissue tissue surrounding the organ, the prefix para (Greek: near): parametritis, etc. is used. To indicate inflammation of the inner membrane, the prefix endo is used (Greek: inside: endocarditis, endometritis). The localization of the inflammatory process in the middle layer of the abdominal organs is indicated by the prefix meso: mesoaortitis. To fully characterize inflammation, it is recommended to indicate the form of its course and type, for example, acute catarrhal gastritis, etc. In the absence of exudative phenomena, the process is designated by adding the end of oz (nephrosis, lymphadenosis) to the Greek name of the organ, and when fibrous connective tissue grows in the organ, the term fibrosis (Latin fibra) is used. 4.4. Classification of inflammation Based on the severity of one of the three main components of the inflammatory process (alteration, exudation, proliferation). Therefore, inflammation is divided into three types: alterative, exudative, proliferative. In turn, each of these types is divided into types and forms, depending on their characteristics. The alterative type of inflammation is divided according to its course into acute and chronic forms, the exudative type - according to the type and location of the exudate, the proliferative type - according to the extent of the process (diffuse and focal form). 4.5. Inflammation classification scheme Table 1 Inflammation Alterative type Exudative type Proliferative type 22 1. Acute form 1. Serous inflammation 1. Diffuse 2. Chronic form A. Serous inflammatory edema 2. Focal B. Serous inflammatory dropsy B. Bullous form 2. Fibrinous inflammation A. Croupous (superficial) B. Diphtheritic (deep) 3. Purulent inflammation A. Abscess B. Empyema C. Phlegmon 4. Hemorrhagic inflammation 5. Catarrhal inflammation 6. Putrefactive ( gangrenous, ichorous) inflammation Questions for self-control 1. Serous-inflammatory edema, macro- and micropicture. 2. Serous-inflammatory dropsy, macro- and micropicture. 3. Fibrinous inflammation, macro- and micropicture. 4. Purulent inflammation, macro- and micropicture. 5. Catarrhal inflammation, macro- and micropicture. 6. Proliferative inflammation, macro- and micropicture. 7. Alternative inflammation, macro- and micropicture.