Tumor Maria Sayarajdbsjahwhegvenkohvs.pptx

About cancer and tumor

1. Tumors Maria Sayar General Medicine 222i1b Pathophysiology free work

2. Neoplasia is a typical pathological process that does not submit to the regulatory mechanisms of the body and is characterized by unlimited cell proliferation. The formation of tumor tissue is characterized by a disorder of the genetic control of the cell cycle due to the action of various oncogenic factors. Overgrowth of tumor tissue is a local manifestation of a common tumor disease of the body. In general benign tumors are designated by attaching the suffix — oma to the cell type from which they arise (for example, myoma , osteoma , chondroma , fibroma, etc.). Malignant tumors arising from epithelial tissue are called cancer, or carcinoma, from connective tissue — sarcoma. A large number of tumors are called using the organ in which they were formed ( hepatoma , thymoma , etc.). Tumors are divided into benign and malignant

3. Benign tumors consist of differentiated cells, in these tumors, morphological atypicalness occurs only at the tissue level, they do not have cellular atypicalness . Benign tumors grow expansively, their borders are even, smooth, limited by the capsule, they develop slowly, pushing the surrounding tissue, do not penetrate into the tissue, do not metastasize, the metabolism in them does not differ from the metabolism in healthy tissues, rarely recur. Malignant tumors consist of cells with low differentiation or undifferentiated cells; have biochemical, cellular and tissue atypicalness . They are characterized by invasive, rapid growth, they penetrate into surrounding tissues and, due to the absence of capsule, do not have clear borders, give metastases and relapses. Perverted metabolism in the malignant tumors leads to cachexia of the body. There are tumors that occupy an intermediate position between benign and malignant tumors. They are called carcinoma in situ. Carcinoma in situ has a number of atypicalness characteristics of malignant tumors, however, due to the presence of the capsule, it does not grow invasively and does not metastasize. But after a certain time, due to additional mutations, these tumors acquire new properties — invasiveness and the ability to metastasize. Etiology of tumors. The factors that cause the formation of tumors are called carcinogens (forming a tumor). These factors acting on the genes of a normal cell, lead to mutations in the genes involved in cell division. As a result of the action of carcinogenic factors, a normal cell is transformed into a tumor (neoplastic) cell. Exogenous and endogenous carcinogenic factors are distinguished. Exogenous carcinogenic factors include physical, mechanical, chemical, and biological carcinogens. Among the physical carcinogens various types of ionizing radiation (x-rays, gamma rays, etc.) and ultraviolet rays are of great importance. These factors, directly affecting the DNA molecule, disrupt its structure (gene mutation, chromosomal aberration). Regular intake of very hot food (thermal factor) plays a large role in the formation of malignant tumors of the oral mucosa. As a result of prolonged mechanical irritation in the stomach, lungs, rectum and other organs, malignant tumors can form. Among the etiological factors of malignant tumors, chemical carcinogens play a leading role. According to WHO, 80% of all tumors are caused by chemical carcinogens. Chemical carcinogens are compounds that can pass through the cell membrane and, entering the cell nucleus, enter into a chemical reaction with nucleotides.

4. Among the etiological factors of malignant tumors, chemical carcinogens play a leading role. According to WHO, 80% of all tumors are caused by chemical carcinogens. Chemical carcinogens are compounds that can pass through the cell membrane and, entering the cell nucleus, enter into a chemical reaction with nucleotides. Chemical carcinogens are divided into organic and inorganic. Chemical carcinogens are also divided into direct and indirect types of action. Carcinogens that have a direct effect, without undergoing any transformations in the body, directly affect the genetic apparatus of the cell and lead to the development of tumors. Such compounds include chloroethylamines , epoxides, alkylating compounds, some antitumor compounds (for example, cyclophosphamide), acetylating factors (1-acetyl-imidazole) and others. Indirect carcinogens can cause an effect after a series of metabolic transformations in the body. This group of compounds includes polycyclic aromatic hydrocarbons, aromatic amines, nitroso compounds and nitramines , aflatoxins, etc. For example, epoxides are formed from polycyclic aromatic hydrocarbons, hydroxyamines — from aromatic amines, and alkaline radicals — from nitrosamines.

5. The formation of a blood and clot is coagulation associated mechanisms of hemostasis. The basis of the vascular-platelet mechanism is a violation of the integrity of the vessel wall and an increase in the ability of platelets to adhere and aggregate. The main reason for platelet adhesion is deendothelization of the vascular wall as a result of its damage (fig. 9.2). As a result of this, a special protein located on the subendothelial | A layer, von Willebrand factor, connecting with receptors on the surface of platelets (glycoprotein Ib — Gp Ib ), provides platelet adhesion. Activated platelets and from damaged tissues release substances that provide high platelet aggregation ability (ADP, thromboxane Az , etc.). Under the influence of these substances, other receptors located on the platelet surface ( GplIb / IIla ) undergo conformative changes and, through fibrinogen bridges, other platelets are also involved in this process. Thus, a “plug” is formed, consisting of aggregated platelets. Aggregated (activated) platelets _ release procoagulants (thromboplastins), what initiates the stage of coagulation of thrombosis.

6. There are 2 ways of coagulation: intrinsic and extrinsic. The intrinsic pathway begins with the activation of the XII coagulation factor (Hageman’s factor), and the extrinsic pathway begins with the activation of cellular lipoproteins called tissue factor (VII coagulation factor). Both pathways lead to the activation of the X factor, as a result, prothrombin converts to thrombin. In turn, small molecule peptide chains are separated from the fibrinogen molecule under the action of thrombin and it leads to the formation of fibrin. Under the action of the fibrin-stabilizing factor (factor XIII), the formed fibrin monomers polymerize and turn into insoluble fibrin filaments. Then a certain amount of plasma is separated from the thrombus, its volume decreases, i.e. thrombus retraction occurs. Fibrin formed on the damaged areas of blood vessels under the action of fibrinolysin (plasmin) is rapidly hydrolytically cleaved.

7. ccording the composition there are white, red, mixed and hyaline thrombi. The white thrombus is formed mainly in the arteries, consists of platelets, fibrin filaments and white blood cells. The red thrombus most often forms in the veins, contains platelets, fibrin filaments and a large number of red blood cells. The mixed thrombus has a multi-layered, stepped structure, the head part resembles white, the body resembles a mixed one, and the tail part resembles a red thrombus; found in veins, in the area of aortic aneurysm, in the cavities of the heart. Hyaline thrombus consist of precipitated plasma proteins, leucocytes and splited erythrocytes and platelets; found in the microcirculation system, mainly during infectious and septic processes.

8. outcomes of thrombosis . Arterial thrombosis leads to ischemia, and vein thrombosis leads to venous congestion. The possible outcomes of thrombosis are (fig. 9.3): > autolysis. Blood clots can undergo septic and aseptic autolysis. Under favorable conditions, small thrombus under the action of fibrinolysis and non-specific plasma proteases completely melt (aseptic autolysis). When pyogenic bacteria enter into the blood clot, septic autolysis occurs; > blockage ( obturation ) of the vessel lumen by a thrombus at the place of its formation; > thromboembolism. All blood clots can lead to embolism. Thromboembolism occurs as a result of the separation of a thrombus or part of it from the vessel wall; > organization and recanalization (vascularization). Over time, in the area of attachment of a thrombus to the vascular wall, endothelial and smooth muscle cells, fibroblasts proliferates inside the thrombus, that leads to the organization of thrombus. In turn, this leads to a thickening of the vascular wall in this area. Then, channels are formed in the thrombus. These channels lined with endothelial cells, i.e. thrombus recanalization occurs. Sometimes calcium compounds precipitate in the area of thrombosis (petrification). In this case, stones can form in the walls of the veins ( phlebolitis ). In areas where collateral circulation is not developed, blockage of the vessel with a thrombus can lead to necrosis (infarction). The role of coronary artery thrombosis in the development of myocardial infarction is especially great. Atherosclerosis, obliterating endarteritis, diabetes mellitus are risk factors for thrombosis in arteries.

9. Embolism: Occlusion of the lumen of the vessel with unusual particles brought by the blood and lymph flow is called embolism, and these particles are called emboli. By origin emboli are divided into 2 groups — endogenous and exogenous. According to localization, ‘emboli of the greater and lesser circulation are distinguished, as well as emboli of the portal vein system. Retrograde emboli are very rare. In this case, emboli, not obeying the laws of hemodynamics, under their weight move in the opposite direction to the bloodstream (for example, with a decrease in the suction force of the chest). A paradoxical embolism occurs when the embolus moves through the veins of a systemic blood circulation and when it enters from the right ventricle, by passing the pulmonary blood circulation, into the left ventricle. This occurs during the interventricular septal defect.

10. Exogenous emboli include air, gas, bacterial and foreign body embolism. Air embolism occurs during damage of the veins (jugular, subclavian, etc.). This is due to negative pressure in the veins and a weak contractile characteristic of these veins. Gas embolism develops mainly during the work in caisson conditions, for example, for divers (during a rapid transition from an environment with high atmospheric pressure to normal conditions), as well as during depressurization of aircraft. Microbial embolism occurs as a result of entering of microorganisms, fungi, parasites ( echinococcus ) into the general bloodstream. Cleavage of the infected thrombus may also result in microbial embolism. Bacterial embolism leads to the formation of abscesses in the area of occlusion of the vessel.

11. Endogenous embolism includes thromboembolism, fatty, tissue embolism and amniotic fluid embolism. Thromboembolism is the most frequently observed type of embolism that occurs as a result of the separation of a thrombus or part of it from the vessel wall (due to aseptic or purulent autolysis). Thromboembolism is most common in the pulmonary arteries (20%), rarely in the portal vein. Occlusion of small branches of the pulmonary artery leads to the development of hemorrhagic infarction in the lungs, and occlusion of large branches or trunk of the pulmonary artery leads to sudden death. The cause of sudden death is the occurrence of a pulmonary coronary reflex /2/. So, during thromboembolism of the pulmonary artery, richly equipped with nerve receptors, their severe irritation occurs, which leads to a simultaneous spasm of the bronchi, branches of the pulmonary artery and coronary arteries and reflex cardiac arrest.

12. Arterial thromboembolism develops during the myocardial infarction, bacterial endocarditis, and atherosclerosis. Cerebral artery thromboembolism leads to encephalomalacia , mesenteric artery embolism leads to intestinal infarction, renal artery embolism leads to kidney infarction, femoral artery embolism leads to lower limb gangrene. Fat embolism develops as a result of droplets of fat entering the blood vessels during a violation of the integrity of the latter. The penetration of bone marrow structures during a fracture of long tubular bones, as well as drops of fat during damage of the subcutaneous fat and burns, into the general bloodstream leads to fat embolism. In some cases, erroneous intravenous injection of drugs prepared on a fat basis can also lead to fat embolism. Droplets of fat through the lymphatic and venous circulation systems enter to the lungs. Here, the small emboli are split by lipase, and large emboli are not completely split and, due to occlusion of the pulmonary arteries of the lungs occur pulmonary infarction.

13. Amniotic fluid embolism develops when the placenta is separated during childbirth as a result of the amniotic fluid entering nearby damaged uterine vessels. On the one hand, the entry of amniotic fluid into the mother’s bloodstream leads to an acceleration of coagulation as a result of the action of thrombokinase , and on the other hand, as a result of the activation of fibrinolytic factors, the amniotic fluid embolism leads to acceleration of fibrinolysis. Vasoactive substances are activated and DIC (disseminated intravascular coagulation syndrome) develops. Tissue embolism develops as a result of damage of various body tissues. Most tissue embolisms are malignant tumor tissues and their metastases.

14. Usually the embolus moves in the circulatory system in 3 directions: + From the veins of the greater circulation and from the right half of the heart in the direction of the arteries of the pulmonary circulation. Pulmonary embolism leads to reflex vasospasm, increased pressure in the pulmonary circulation and decreased pressure in the systemic circulation. Hemodynamic changes cause an increase of the central venous pressure (CVP) in the vena cava superior or in the right ventricle, acute right ventricular failure and death; + The movement of the embolus from the left half of the heart, aorta and large arteries in the direction of the organs. Pathological processes in the left half of the heart ( thromboendocarditis , myocardial infarction, etc.), thrombosis in the arteries of the systemic circulation, gas and fat embolism, etc. constitute the basis of embolism of the systemic circulation; % Embolism of the portal vein of the liver is manifested by severe hemodynamic disorders. Occlusion of the portal vein of the liver and its branches ( v.mesenterica superior, v.lienalis , v.gastrica ) by an embolus leads to congestion in the abdominal organs (stomach, intestines, spleen) and the development of portal hypertension.

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