Presentation on the topic "atherosclerosis". Concept of atherosclerosis

Presentation on the topic: Atherosclerosis

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Atherosclerosis is a common chronic disease of arteries of the elastic and muscular-elastic type (large and medium caliber), characterized by the infiltration of atherogenic apoprotein-B-containing lipoproteins into the vessel wall with the subsequent development of connective tissue, atheromatous plaques, organ and general circulatory disorders.

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RISK FACTORS: Socio-cultural: consumption of high-calorie foods rich in saturated fat and cholesterol, sedentary lifestyle, nervous stress. Internal risk factors: arterial hypertension, hypercholesterolemia, impaired carbohydrate tolerance, obesity, family history, others.

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RISK FACTORS: Irreversible – age, male gender, genetic predisposition. Reversible – smoking, hypertension, obesity. Partially reversible - hyperlipidemia, hyperglycemia, low HDL levels, low physical activity, stress.

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Pathological anatomy early atherosclerotic changes in the intima fatty lesions of the intima (fatty streak, lipofibrous plaque) fibrous plaque

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The main pathogenetic mechanisms of exacerbation of atherosclerosis: weakening of the fibrous membrane of the plaque and its rupture; disproportionately large lipid core; thrombus formation at the site of rupture of the plaque capsule or on an endothelial defect with severe stenosis; endothelial dysfunction (local and generalized); diffuse inflammatory reaction.

Presentation Atherosclerosis

Presentation subject: Biology

Topic: Atherosclerosis

Availability of a plan - lesson notes: No

The presentation has been prepared for a detailed study of the common chronic disease of the elastic and muscular-elastic arteries. Objectives of the presentation: To find out the main pathogenetic mechanisms of exacerbation of atherosclerosis.

The term “atherosclerosis” comes from two Latin words: athere - which means mush, and sclerosis - hard, dense, which reflects the stages of development of an atherosclerotic plaque. Atherosclerosis occurs in all people. The first signs of atherosclerosis are detected at the age of five. “Atherosclerosis is a natural aging process” A. Davydovsky

Risk factors for the development of atherosclerosis Gender. Men are more susceptible to developing atherosclerosis than women. The first signs of this pathology can appear as early as 45 years of age, or even earlier, in women - from 55 years of age. This may be due to the more active participation of estrogens and low- and very low-density lipoproteins in the metabolism of cholesterol.

Heredity. This is one of the reasons for the appearance of atherosclerosis. Atherosclerosis is a multi-cause disease. Therefore, hormonal levels, hereditary disorders of the plasma lipid profile, and the activity of the immune system play important roles in accelerating or slowing down the development of atherosclerosis.

Bad habits. Smoking is poison for the body. This habit is another reason for the development of atherosclerosis. As for alcohol, there is an interesting dependence: drinking small doses of alcohol daily is an excellent prevention of atherosclerosis. True, the same dose also contributes to the development of liver cirrhosis. In addition, large doses of alcohol accelerate the development of atherosclerosis.

Nutrition. Our future health will depend on how healthy our food is, how much it contains the chemical compounds we need. Few people know that not a single diet, except for therapeutic ones, is approved by the World Council of Food Hygiene. You need to eat rationally and adequately to your needs and energy costs.

Symptoms of atherosclerosis are often cold, bluish-white extremities; frequent heart problems; memory loss; disturbance of blood supply; poor concentration; the patient becomes irritable and feels tired. People with high blood pressure, weak kidneys and diabetes are more susceptible to atherosclerosis than other people.

Doctors consider atherosclerosis to be the most typical today: of the aorta, causing angina pectoris; kidney; limbs; coronary arteries (coronary heart disease); extracranial vessels, mainly the carotid artery, leading to cerebrovascular diseases and cerebral strokes.

Step 1 Reduce the level of cholesterol and “bad” lipoproteins: exclude spicy, fatty, smoked, canned foods and processed foods; We cook or stew food rather than fry We consume fats only of vegetable origin We exclude products made from premium flour

To drink or not to drink? It's better not to drink alcohol at all! When drinking alcoholic beverages, give preference to white and red wines of weak and medium strength, but no more than 1 glass. An alternative to alcohol is bread kvass, containing from 0.5 to 2.5% alcohol.

To maintain the body and prevent atherosclerosis, you should eat foods low in salt and cholesterol. Eat grains, vegetables, for example: carrots, eggplants, leeks, garlic, boiled fish, yoghurts, sunflower oil and any fruits. Eat large quantities of berries and plants of yellowish-red flowers - for example, hawthorn, rowan, strawberry, viburnum, tansy, etc. To maintain the body and prevent atherosclerosis, you should eat foods low in salt and cholesterol. Eat grains, vegetables, for example: carrots, eggplants, leeks, garlic, boiled fish, yoghurts, sunflower oil and any fruits. Eat large quantities of berries and plants of yellowish-red flowers - for example, hawthorn, rowan, strawberry, viburnum, tansy, etc.

The work can be used for lessons and reports on the subject "Biology"

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Atherosclerosis is a chronic disease of the arteries, accompanied by the formation of single and multiple lipid, mainly cholesterol, deposits or plaques in the inner lining of the arteries.

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Atherosclerosis, or rather increased blood cholesterol, is one of the main risk factors for the development of cardiovascular diseases... this is the “RUST OF LIFE”

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Causes of atherosclerosis The causes of atherosclerosis are high blood pressure, smoking, diabetes, and high cholesterol. But the main cause of atherosclerosis lies in the disruption of cholesterol metabolism.

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Age. This is a natural risk factor. With age, atherosclerotic manifestations worsen.

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Excess weight. This factor has a very negative effect on atherosclerosis. Excess weight can lead to diabetes, and this pathology is very malignant for the development of atherosclerosis.

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How to treat atherosclerosis? Quitting smoking Physical activity Normalizing body weight Maintaining normal blood pressure Changing your diet

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1. Educational institutions “Mozyr State Medical College” “Atherosclerosis”. Prepared by: Beaver Alina. Group: MDD-41. Teacher: Dunayskaya N.E.
2. Atherosclerosis. - a chronic disease of the arteries of the elastic and muscular-elastic type, resulting from disturbances in lipid and protein metabolism and accompanied by the deposition of cholesterol and some fractions of lipoproteins in the intima of blood vessels. Deposits form in the form of atheromatous plaques. The subsequent proliferation of connective tissue in them (sclerosis), and calcification of the vessel wall lead to deformation and narrowing of the lumen, up to obstruction (blockage). Atherosclerosis of the heart vessels leads to the development of coronary heart disease.
3. Epidemiology. The most studied mortality rates from cardiovascular diseases are a manifestation of generalized atherosclerosis. In the Republic of Belarus in 2013, the standardized mortality rate from diseases of the circulatory system was 800.9 per 100,000 population. For comparison, in France this figure is 182.8 (the lowest in Europe), in Japan - 187.4. It has been proven that the reduction in the risk of cardiovascular diseases in these countries is associated not so much with the quality of medical care, but with lifestyle and dietary habits.
4. History. In 1755, Heller introduced the term “atheroma” to describe vascular lesions. In 1761, Morgagni described characteristic hardening of the arteries at autopsy. In 1769, Pouletier de la Salle obtained a dense white substance (“adipose wax”) from gallstones, which had the properties of fats. Cholesterol was isolated in its pure form by the chemist, member of the National Convention and Minister of Education Antoine Fourcroy in 1789. In 1815, Michel Chevreul, who also isolated this compound, called it cholesterol (“chole” - bile, “sterol” - fatty). In 1833, Lobstein introduced the concept of “arteriosclerosis.” 1908 - Ignatovsky and Saltykov for the first time experimentally reproduced atherosclerosis in rabbits, feeding them milk and eggs 1913 - major domestic pathologists Anichkov Nikolai Nikolaevich (later academician of the Academy of Sciences and the Academy of Medical Sciences of the USSR, president of the Academy of Medical Sciences of the USSR) and Khalatov Semyon Sergeevich in their classic works “proved” A direct dependence of atherosclerosis on cholesterol, causing this disease in animals fed with pure cholesterol. However, numerous modern studies conducted in the USA and Europe have not revealed a correlation between the severity of atherosclerosis and blood cholesterol levels. In addition, it has been shown that artificial or pathological reduction of cholesterol levels in the blood significantly increases the risk of developing cancer.
5. Etiology. At the moment, there is no single theory of the occurrence of this disease. The following options, as well as their combinations, are put forward:  theory of lipoprotein infiltration - primary accumulation of lipoproteins in the vascular wall,  theory of endothelial dysfunction - primary violation of the protective properties of the endothelium and its mediators,  autoimmune - primary dysfunction of macrophages and leukocytes, their infiltration of the vascular wall,  monoclonal - primary occurrence of a pathological clone of smooth muscle cells,  viral - primary viral damage to the endothelium (herpes, cytomegalovirus, etc.),  peroxide - primary violation of the antioxidant system,  genetic - primary hereditary defect of the vascular wall,  chlamydia - primary damage to the vascular wall chlamydia, mainly Chlamydia pneumoniae.  hormonal - an age-related increase in the level of gonadotropic and adrenocorticotropic hormones leads to increased synthesis of the building material for hormones - cholesterol.
6. Risk factors:  Smoking (the most dangerous factor).  Hyperlipoproteinemia (total cholesterol > 5 mmol/l, LDL > 3 mmol/l, Lp(a) > 50 mg/dl).  Arterial hypertension (systolic blood pressure > 140 mm Hg; diastolic blood pressure > 90 mm Hg).  Diabetes mellitus.  Obesity.  Sedentary lifestyle (hypodynamia).  Emotional stress.  Poor nutrition.  Hereditary predisposition.  Postmenopause.  Hyperfibrinogenemia.  Homocysteinuria.
7. Risk factors:
8. Risk factors:
9. Atherosclerosis occurs most frequently in men aged 50-60 years and in women over 60 years of age. Progression of atherosclerosis.
10. Smoking. The delivery of oxygen to the heart muscle due to smoking is sharply disrupted due to the blocking of blood hemoglobin by carbon monoxide from tobacco smoke. This leads to serious various damage to the heart and blood vessels.  Among the most toxic substances to the body that come with tobacco smoke is carbon monoxide. It significantly increases cholesterol levels in the blood and causes the development of atherosclerosis. Fats begin to deposit in the arteries supplying the heart, which increases the risk of a heart attack. In addition, the chemicals contained in cigarette smoke, entering the blood, damage the walls of blood vessels, contributing to the formation of atherosclerotic plaques.  It has been proven that the degree of damage to arterial walls by atherosclerosis in smokers is two to three times higher than in non-smokers.
11. Excess body weight.
12. Dyslipidemia. – disruption of the metabolism of lipoproteins and fats, which leads to a change in their content in the blood (increase or decrease). Dyslipidemia is considered as the main factor in the development of atherosclerosis (mainly due to impaired cholesterol metabolism), which in turn can cause the development of hypertension, myocardial infarction and stroke. In patients with diabetes mellitus, increased levels of triglycerides and low-density lipoproteins, as well as decreased levels of high-density lipoproteins, are one of the most important risk factors for cardiovascular complications.
13. The main lipids present in human blood are triglycerides and cholesterol. In its free state, cholesterol does not enter the bloodstream, but first binds to proteins, forming molecular complexes - lipoproteins. There are high-density lipoproteins (HDL) and low-density lipoproteins (LDL). HDL (good cholesterol) - are not deposited on the walls of blood vessels and organs and are important compounds for maintaining normal functioning of the body. LDL (bad cholesterol) can be deposited on the walls of blood vessels, forming so-called cholesterol plaques, which leads to blockage of blood vessels and subsequently atherosclerotic changes. Plasma lipid metabolism. Inhibition of cholesterol synthesis.
14. Pathogenesis.
15. The pathogenesis of atherosclerosis is called atherogenesis. It occurs in several stages. The development of atherosclerotic lesions is a set of processes of lipoproteins and leukocytes entering and leaving the intima, cell proliferation and death, formation and restructuring of the intercellular substance, as well as vascular proliferation and calcification. These processes are controlled by many signals, often in different directions. More and more data are accumulating on the complex pathogenetic relationship between changes in the function of the cells of the vascular wall and the leukocytes that migrated into it and risk factors for atherosclerosis.
16. Atherocalcinosis. Ulceration. Atheromatosis. Liposclerosis. Lipoidosis. Pre-lipid. Stages of disease development:
17. Prelipid stage. It is characterized by the fact that microscopically the intima of the arteries looks normal. But at this stage metabolic disorders are noted. They manifest themselves in:  Macroglobulinemia.  Hypercholesterolemia.  Appearance of low density lipoproteins.  Violation of mineral metabolism.  Activation of hyaluronidase. In the intima in the prelipid stage, microscopic and electron microscopic examination reveals mucoid edema, accumulation of acidic mucopolysaccharides, foam cells-macrophages, in the cytoplasm of which fats and cholesterol accumulate.
18. Stage of lipoidosis. At this stage, gray-yellow spots visible to the naked eye appear in the intima, slightly rising above the surface. The size of the spots ranges from 1 to 2 cm in diameter. Localization of lipid stains - aorta, coronary arteries, arteries of the lower extremities, kidneys, etc. There are especially many of them in the aorta and places where arteries branch, which is associated with increased blood pressure in these areas. Microscopically, in areas of pathology the following are noted:  foamy xanthoma cells.  accumulations of lipids in the stroma outside the cells.  destruction of elastic, collagen, reticular fibers and smooth muscle cells.
19. Stage of liposclerosis. It is characterized by the appearance of fibrous plaques in place of lipid stains. The sizes of fibrous plaques are varied, often corresponding to the size of lipid spots. Shape: round, oval, striped. A distinctive feature is that plaques rise above the surface of the intima, which leads to a narrowing of the lumen of the artery. The number of plaques varies widely. They can be single or numerous. Microscopic examination in the area of the fibrous plaque reveals:  proliferation of fibrous tissue.  Numerous foam cells.  lipid accumulations.  destruction of the elasto-muscular framework.  smooth muscle cells.  microvessels growing from the tunica media into the intima.
20. Stage of atheromatosis. At this stage, a large amount of lipids, cholesterol, and proteins accumulate in the center of the plaque. This entire lipid-protein mass is a gray-yellow mushy substance, reminiscent in appearance of the contents of atheromas. Microscopically, the affected area of the artery is a powerful fibrous plaque of considerable size, which significantly narrows the lumen of the arteries.  Especially many of these plaques are observed in the abdominal aorta. Tissue detritus in the center of the plaque consists of cholesterol crystals, xanthoma cells, and fragments of destroyed vessel structures.
21. An ulcer forms. The contents of the ulcer are washed out by the blood and spread throughout the body, which can cause blockage of microvessels and tissue damage due to ischemia. Thrombotic masses and foci of hemorrhage appear at the bottom of the ulcer. Microscopic examination of the pathological area allows us to identify:  accumulations of lipids, cholesterol, proteins.  destruction of collagen fibers.  accumulations of lymphocytes, plasma cells, xanthoma cells  deep defects.  ulceration of the arterial wall up to the adventitia (this is a complicated variant of atherosclerosis). Ulceration stage. Ulcerated atheromatous plaque of the aorta with mural thrombosis.
22. Stage of atherocalcinosis. It is characterized by calcium deposition at the site of the atherosclerotic and atheromatous process. This process can occur in all affected arteries, but it is especially pronounced in the lower aorta. Lime deposition is promoted by aspartic and glutamic acids. When the pathology focus is calcified, the damaged artery wall is strengthened. But the artery loses the ability to change its lumen in response to fluctuations in function.
23. Fig.1. Edema of the coronary artery in a young man of 18 years. Fig. 2. Fibrinous film on the surface of the unchanged inner lining of the coronary artery in a 32-year-old man. Rice. 3. Splitting and fragmentation of the internal elastic membrane in the coronary artery (left) in the area of muscular-elastic thickening of the inner membrane and in the aorta (right) in the area of the rhythmic structure. Rice. 4. Proliferation of smooth muscles with the formation of a longitudinal layer (upper third of the figure) in the inner lining of the coronary artery. Rice. 5. Obesity of smooth muscle fibers in the area of muscular-elastic thickening of the inner lining of the coronary artery. Top right and center - formation of free drops of fat. Rice. 6. Same as in Fig. 5 in the area of the rhythmic structure of the aorta. Bottom right - different stages of smooth muscle fiber obesity; The arrow indicates a dead cell with the release of fat. Rice. 7. Lipid plaque in the coronary artery Fig. 8. Walled-up masses of fibrin in the cover of an atherosclerotic plaque. The deep layers of the plaque are saturated with protein-rich liquid. Rice. 9. Old atherosclerotic plaque with cholesterol crystals and atheromatosis in the center and deposition of calcium salts - lower right.
24. Symptoms of atherosclerosis: The deposition of cholesterol in the arterial wall is accompanied by a compensatory bulging outward, due to which there are no obvious symptoms of atherosclerosis for a long time.  With atherosclerosis of the thoracic aorta, intense burning pain appears behind the sternum, radiating to the neck, back, and upper abdomen. With physical activity and stress, the pain intensifies.  Atherosclerosis of the abdominal aorta is characterized by abdominal pain, bloating, and constipation. With atherosclerotic lesions of the aortic bifurcation (the place where the aorta divides into branches), Leriche syndrome develops with such manifestations as: intermittent claudication, coldness of the lower extremities, impotence, toe ulcers.  Atherosclerosis of the mesenteric vessels is manifested by sharp, burning, cutting pain in the abdomen during meals, lasting 2-3 hours, bloating, and stool disturbances.  Atherosclerosis of the renal arteries is characterized by a persistent increase in blood pressure, changes in urine analysis.  Atherosclerosis of the peripheral arteries is manifested by weakness and increased fatigue of the leg muscles, a feeling of chilliness in the limbs, intermittent claudication (pain in the limbs appears while walking, forcing the patient to stop).
25. Biochemical blood test for atherosclerosis: 1. Triglycerides in blood serum. 2. Total cholesterol in blood serum. 3. Serum high-density lipoprotein (HDL) cholesterol. 4. Low-density lipoprotein (LDL) cholesterol in blood serum. 5. Index or coefficient of atherogenicity. All of the above indicators will be deviated from the norm. Normal lipid profile indicators are as follows:  total cholesterol - less than 200 mg/dl (5.2 mmol/l)  HDL cholesterol - more than 50 mg/dl (1.3 mmol/l)  LDL cholesterol - less than 130 mg/dl (3.4 mmol/l)  triglycerides - less than 250 mg/dl (2.3 mmol/l)  atherogenic index - 3–3.5 points.
26. Diagnostics.  Questioning the patient and identifying the symptoms of the disease: symptoms of coronary heart disease, symptoms of cerebrovascular accident, intermittent claudication, symptoms of abdominal angina, etc.;  General examination of the patient: signs of aging of the body, listening to systolic murmur in the aorta; It is necessary to palpate all arteries accessible to palpation: the aorta, external iliac arteries, common femoral arteries, popliteal arteries, arteries of the dorsum of the foot and posterior tibial artery, radial and ulnar arteries, carotid arteries.  Determination of systolic murmur over auscultatory points of arteries.  If there is a suspicion of damage to the arterial bed of the lower extremities, determine the capillary response.  Determination of cholesterol concentration in the blood and determination of blood lipid balance;  X-ray examination of the chest organs, x-ray endovascular examination methods;  Ultrasound examination of the heart and abdominal organs and retroperitoneal space;  Dopplerography of the vessels of the extremities or, what might be better, ultrasound duplex and triplex scanning of the arteries of the brachiocephalic region, arteries of the lower extremities, aorto-iliac segment, as well as transcranial Doppler.
27. Drug treatment of atherosclerosis. Drug therapy for atherosclerosis involves the use of 4 groups of hypolipidemic (lipid level-lowering) drugs:  Bile acid sequestrants  Nicotinic acid.  Fibrates.  Statins. These agents have a stabilizing effect on the atherosclerotic plaque, improve the function of the endothelium (the inner lining of blood vessels), and inhibit the development of atherosclerosis, while differing in the severity of their effect on various indicators of lipid metabolism. Only the attending physician will recommend the necessary drug and its dosage.
28. Treatment. Non-drug methods for correcting hyperlipidemia:  smoking cessation.  refusal of alcohol.  refusal of fried foods.  refusal of fatty animal foods.  refusal of red meat (beef, pork, lamb).  active lifestyle - regular dosed physical activity.  maintaining psychological and physical comfort.  loss of body weight. Physical activity for atherosclerosis. Prevention: Increasing physical activity has a positive effect for patients with atherosclerosis. Patients without clinical manifestations of atherosclerosis are advised to exercise for 40 minutes daily. The intensity of the exercise should be 60% of the maximum heart rate (calculated = 220 - age). Walking, swimming, dancing are useful - moderate intensity 60-90 minutes per week. Isometric (power) loads are unacceptable. It is recommended to use any opportunity for physical activity: walking, using a car less often.
33. Remember: “It is better to prevent a disease than to treat it later”!

Presentation on the topic "atherosclerosis". Concept of atherosclerosis

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