Animal anatomy, histology, pathological anatomy

LITERATURE
1. Belkin, B. L. Pathological diagnosis of animal diseases (with the basics of autopsy and forensic veterinary examination): textbook / B. L. Belkin, V. S. Prudnikov. – Orel: OSAU, 2007. – 368 p. 2. Animal diseases (with the basics of pathological diagnosis and forensic veterinary examination) / V. S. Prudnikov [et al.]; edited by V.S. Prudnikova. – Minsk: Technoperspective, 2010. – 507 p. : [16] l. color ill. 3. Autopsy of animals and differential pathomorphological diagnosis of diseases: textbook / M. S. Zhakov [et al.]. – Minsk: Urajai, 1998. – 263 p. : ill. 4. Zharov, A.V. Autopsy and pathomorphological diagnosis of animal diseases: a textbook for university students specializing in “Veterinary Medicine” / A.V. Zharov, I.V. Ivanov, A.P. Strelnikov; ed. A. V. Zharov. – Moscow: KolosS, 2003. – 400 p. : ill. 5. Zharov, A.V. Forensic veterinary medicine / A.V. Zharov. – 2nd ed., revised. and additional – Moscow: Kolos, 2007. – 320 p. 6. Pathological anatomy, autopsy and forensic examination: educational manual / V. S. Prudnikov [etc.]. – Vitebsk: OU VGAVM, 2008. – 28 p. 7. Pathological anatomy of farm animals. Workshop: textbook for students of higher agricultural educational institutions in the specialty “Veterinary Medicine” / V. S. Prudnikov [etc.]; edited by V. S. Prudnikova. – Minsk: Information Computing Center of the Ministry of Finance, 2010. – 352 p. : ill. 8. Salimov, V. A. Workshop on pathological anatomy of animals. – Moscow: Kolos, 2003. – 189 p. : ill. 9. Handbook on autopsy and pathomorphological diagnosis of animal diseases (with the basics of forensic veterinary examination) / V. S. Prudnikov [etc.]. – Vitebsk: Educational Institution VGAVM, 2007 – 375 p.

3.2. TRAINING MATERIALS FOR PRACTICAL LESSONS

SUBJECT:CONSTANTIAL HYPEREMIA OF THE LIVER

1. Hyperemia of liver stagnation. Description of the course There may be various circulatory disorders in the body and in individual organs. Hypertension is an increase in the amount of blood in the arteries of overgrown tissue. Depending on the origin, there are different types of arterial and venous bleeding. These disorders are of two types: general and local. The most common local disorders are hyperemia, hemorrhage, hemorrhage, heart attack, thrombosis, as well as embolism and congestion. Arterial hyperemia is an increase in the quantity and quality of blood in the arteries of organs during normal blood flow. At the same time, the blood vessels dilate, the organ becomes red, metabolism increases, and secretion production in the glandular organs increases. Depending on the mechanism of development, there are vasomotor, secondary, inflammatory, and inflammatory. Vasomotor polycystic ovary syndrome is caused by vasoconstrictor or contractile nerve action (cold, heat, chemicals) or paralysis. Collateral polycystic ovary syndrome is a violation of the blood supply to the affected area due to thrombosis and embolism. Vaginal polycystic ovary syndrome is a disease caused by low blood pressure. For example, when a jar is placed on a person's skin, it is more pronounced. Venous thrombosis is a complication of normal blood flow in the arteries. This is also called stagnation. There are acute and chronic venous thrombosis. Acute venous thrombosis is a narrowing of the vein by the upper fetus, which leads to intimal inflammation and thrombosis. It increases organ size, changes color from dark red to blue, and causes tumors in the lungs, gastrointestinal tract, and skin. Chronic venous thrombosis - dystrophy, atrophy, proliferation of connective tissue. Outcomes. Once the cause is identified, bleeding returns, swelling returns, fluid is absorbed and circulation is restored. Polygamy also leads to the development of thrombosis, bleeding and inflammation. It is characterized by stagnation (bleeding) and tissue destruction. Stagnation is a complete cessation of blood flow in organs, tissue capillaries and small veins. This increases the amount of blood in the arteries, red blood cells condense and form a solid mass. Hyaline thrombosis - depending on the mechanism of development, there is a difference between stagnation and true stagnation. Stagnation is caused by slowing blood flow. True stagnation occurs with viral infections and poisoning. This causes red blood cells to clump together and stop blood flow. There are no blood clots in the arteries and the arteries do not dilate. Outcomes. Long-term stagnation is characterized by dystrophic changes characterized by tissue destruction. For example, in the case of erysipelas, these changes are observed with paratyphoid fever. Red blood clots are similar to blood clots that clot after death. It is dark red in color and consists of dense fibers of fibrin, red blood cells and white blood cells attached to meshes. These clots are caused by very slow blood flow. Occurs in the veins during stagnation. Mixed blood clots - the head of the blood clot is made up of platelets that adhere to the wall of the blood vessel. The body of the thrombus is layered, and the tail hangs in the vascular bed. Filled blood clots are found in small veins and capillaries. They block the entire vascular system. This clot is made up of sticky red blood cells and plasma proteins. Occurs in burns and some infectious diseases. In relation to the vessel wall, the following thrombi are distinguished: Layered thrombi are cells that form in damaged endothelial cells when there is no blood flow in large arteries. It consists of platelets, leukocytes and fibrin. Filling clots - occur in small blood vessels, then form in walled blood clots and fill the entire wall of the vessel. Thrombi differ from blood clots in a dead body in that they adhere to the vessel wall. White and mixed thrombi are completely adjacent to the vessel wall. Red blood clots, on the contrary, hang only on the head in the vessel wall and are easily separated. The free surface of the thrombus is uneven, the fibrin threads in the thrombus are thick, and the blood clots in the dead body are thin. Consequences and significance. When a blood clot breaks through a wall and travels through the bloodstream, it can cause an embolism. If it is not broken, it will be destroyed. It involves proteolytic enzymes and purulent microbes. In most cases, the blood clot adheres to the wall of the vessel and is replaced by connective tissue. Some blood clots dry out and become salty. Blood clots cause ischemia, heart attack or gangrene. Embolism is the blockage of blood vessels by foreign substances flowing through the bloodstream. Emboli can be formed from thrombus particles, tissue debris, tumor cells, fat droplets, air or gas bubbles, gels and microbes. Emboli travel through the bloodstream. Emboli can also be directed against the bloodstream. Thromboembolism, caused by rupture of a blood clot, is common in farm animals. They are found in the lungs, kidneys, spleen and intestines. A fat embolism is caused by a rupture of long bones, in which droplets of free fat enter the characteristic veins and move into the pulmonary capillaries with the movement of blood, causing emboli. This is unknown at first, but may occur if emboli form in 3 to 2 parts of the pulmonary capillaries. An air embolism is when air enters a damaged vein. This can also occur with intravenous administration. Different animals react to this differently. For example, horses can pass 10 ml of air per 1 kg of body weight, and rabbits - 2–3 ml of air. Excessive air intake is dangerous because it interferes with blood circulation, dilates the right side of the heart and even causes cardiac paralysis. If an embolism is suspected, the body should be opened immediately (within 1 day). The bladder is easily visible in the pulmonary arteries in the heart cavity. Gives good results when cutting veins in water. Detection of foamy blood in the heart also has diagnostic value. Gas embolism is characterized by the release of dissolved gases into the blood as a result of a decrease in vascular pressure. In an animal it is unknown, it does not matter. But for pilots, this happens when divers go from high pressure to low pressure. (decompression sickness). Parasitic, bacterial and tissue emboli are common in animals. Emboli, consisting of tumor cells and microbial communities, lead to the proliferation of fibrinous processes and the spread of malignant tumors. Outcomes - In many cases, embolism can lead to other diseases. The outcome of emboli depends on their nature, size, number and narrowing of the arteries. Animals may not die from embolism, but degenerative, necrotic processes and heart attacks may occur. A heart attack is a rupture of the hearth that occurs as a result of interruption of blood flow. Its cause is thrombosis, embolism. Heart attacks occur in the kidneys, spleen, heart, intestines and lungs. Narrowing of blood vessel walls (in the coronary arteries) also leads to a heart attack. Heart attacks have a conical shape. Its internal part is exposed to foreign bodies in the vascular bed, and its base is exposed to the surface of the organ. On the cut surface they look triangular. The form of myocardial, intestinal and brain infarction depends on the location of the blood vessels. Heart attacks can be single or multiple. The consistency depends on the type of necrosis and the consistency of the organ. Depending on the color, there are three types of infarction: anemic, red or hemorrhagic and white infarction. Anemic heart attack is caused by contraction of the artery walls. Occurs in the kidneys, spleen, sometimes in the myocardium and intestines. The cut surface is dry, light brown. Microscopy reveals vascular anemia. Hemorrhagic infarction is caused by congestive heart failure. This infarction occurs in the intestines, lungs and myocardium. The cut surface is moist, dark red. It is characterized by filling of microscopic vessels with blood and even accumulation of blood in the interstitial connective tissue. Sometimes red blood cells rupture, causing a hemorrhagic infarction. White infarction depends on the size and anatomical structure of the organ. Some infarcts become limited and resolve, forming a scar of connective tissue. Myocardial infarction can be fatal. Flatulence may be due to an obstruction created by a cancerous tumor. Infarctions in the brain lead to paralysis. These disorders are of two types: general and local. The most common local disorders are hyperemia, bleeding, hemorrhage, infarction, thrombosis and embolism. Hyperemia is an increase in blood in a specific tissue or organ. Venous and arterial hyperemia differ. Congestive hyperemia is common. This congestion is caused by heart failure or lung disease. This hyperemia can be acute or chronic. Macroscopic view. The pungent shape of the liver resembles a nutmeg on the outside - the center of the piece is reddish-brown or blue-red, and the edges are light gray. The organ is enlarged several times, the capsule is tense, and when it is cut, bleeding occurs. In the chronic form, liver cirrhosis may be partially preserved, have a hard consistency and reduced size. The hard consistency is due to the proliferation of connective tissue. Microscopic view. In a small mirror, the focus is, of course, at the center of the particle. The central vein and the capillaries adjacent to it are filled with blood and dilated. At the edges of the segment, the capillaries are close to normal (not dilated). The barriers in the center of the cell narrow and separate from each other, and the cells are scattered. In a large mirror, we focus on the center and edges of the segment. The railing in the center is thin and broken in places. The borders of liver cells are indistinguishable, and their nuclei are small, dark in color, with uneven edges, jagged - pyknosis. Liver cells sometimes contain a yellowish-brown pigment called lipofuscin. This indicates a long-term metabolic disorder. The cells in the middle and along the edges of the section show the role of fat droplets - ring-shaped cells. In the chronic form, there is rod-shaped connective tissue in the center of the segment, and the above-mentioned structural changes are present at the edges.