Presentation on the topic "atherosclerosis". The concept of atherosclerosis. Etiology and pathogenesis of atherosclerosis. Classification of atherosclerosis. Pathological anatomy of atherosclerosis. Complications of atherosclerosis. Modern theories of the formation of atherosclerosis presentation

  • Slide 2

    • Atherosclerosis is chronic illness arteries, accompanied by the formation of single and multiple lipid, mainly cholesterol, deposits or plaques in inner shell arteries.
  • Slide 3

    • Atherosclerosis, or rather increased blood cholesterol, is one of the main risk factors for the development of cardiovascular diseases
    • ... this is “RUST OF LIFE”
  • Slide 5

    Causes of atherosclerosis

    • The causes of the development of atherosclerosis are high pressure, smoking, diabetes, high level cholesterol.
    • But the main cause of atherosclerosis lies in the disruption of cholesterol metabolism.
  • Slide 6

    Risk factors for the development of atherosclerosis

    • Floor. 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.
  • Slide 7

    • Age. This is a natural risk factor. With age, atherosclerotic manifestations worsen.
  • Slide 8

    • Heredity. This is one of the reasons for the appearance of atherosclerosis. Atherosclerosis is a multi-cause disease. Therefore, the level of hormonal levels, a hereditary disorder lipid profile plasma, activity immune system play important roles in accelerating or slowing down the development of atherosclerosis.
  • Slide 9

    • 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.
  • Slide 10

    • Excess weight. This factor has a very negative effect on atherosclerosis. Excess weight can lead to diabetes mellitus, and this pathology is very malignant for the development of atherosclerosis.
  • Slide 11

    • Nutrition. On how healthy our food is, how much it contains what we need chemical compounds, our future health will depend. 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.
  • Slide 12

    Symptoms of atherosclerosis

    • often cold extremities of a bluish-white color;
    • 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.
  • Slide 13

    Stages of development of atherosclerotic plaque

    • Simply put, atherosclerosis begins with cholesterol deposits on the walls of a blood vessel with the formation of an atherosclerotic plaque. This causes the vessel to narrow (stenosis), reducing blood flow through it. At the next stage of development of atherosclerosis, atherosclerotic plaques are destabilized with disruption of the surface and the formation of necrotic zones. It is these zones that attract blood platelets - platelets, resulting in the formation blood clot(thrombus).
  • Slide 14

    • Formation of a blood clot in a vessel, where: 1 - normal look cross section of the vessel; 2 - beginning of plaque formation; 3 - circular deposition of fats in vascular wall; 4 - complete (or partial) cessation of blood flow in the vessel caused by its thrombosis.
  • Slide 15

    • Doctors consider atherosclerosis to be the most typical today: of the aorta, causing angina pectoris; kidney; limbs; coronary arteries ( ischemic disease hearts); extracranial vessels, mainly carotid artery, leading to cerebrovascular diseases and cerebral strokes.
  • Slide 16

    How to treat atherosclerosis?

    • To give up smoking
    • Physical activity
    • Normalization of body weight
    • Support normal blood pressure
    • Changing your diet
  • Slide 17

    Step 1

    • We reduce the level of cholesterol and “bad” lipoproteins:
    • exclude spicy, fatty, smoked, canned foods and semi-finished products;
    • We boil or stew food rather than fry it
    • We consume fats only of plant origin
    • We exclude products made from premium flour
  • Slide 18

    Step 2

    • We increase the level of “good” lipoproteins:
    • More seafood
    • We regularly exercise
  • Slide 19

    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.
    • Alternative to alcohol - bread kvass, containing from 0.5 to 2.5% alcohol.
  • Slide 20

    • 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 fruit. IN large quantities eat berries and plants of yellowish-red flowers - for example, hawthorn, rowan, strawberry, viburnum, tansy, etc.
  • Slide 21

    • Thank you for your attention))
    • Be healthy!
  • View all slides

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    Presentation on the topic: Atherosclerosis

    Slide description:

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

    Slide description:

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

    Slide description:

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

    Slide description:

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

    Slide description:

    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 illness arteries of elastic and muscular-elastic type. Objectives of the presentation: To find out the main pathogenetic mechanisms of exacerbation of atherosclerosis.

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    A chronic disease characterized by a violation of fat and protein metabolism, which is manifested by the deposition of protein-lipid complexes in the walls of vessels of the elastic and muscle-elastic type and, in connection with this, the development of sclerotic changes there. Atherosclerosis is a type of arteriosclerosis.




    Endothelium Elastic membrane Smooth muscle cells 1. Prelipid stage. Endocrine and metabolic disorders. Local reasons helping to increase vascular permeability for fat and protein substances. Destructive changes in the vascular endothelium. Pathomorphology - fat-containing vacuoles appear in the cytoplasm of endothelial cells. The basement membrane is fragmented, elastic and collagen fibers are destroyed.




    2. Stage of fatty spots and streaks (lipidosis). focal accumulation of fat-protein deposits in the intima of vessels; in these foci, macrophages appear that carry out phagocytosis. (xanthoma cells) Pathomorphology: spots and stripes yellow color clearly visible during visual observation. Spots and stripes do not rise above the surface of the vessel and do not change its elasticity.


    3. Stage of fibrous plaque (liposclerosis). development of connective tissue and new formation of blood vessels in the plaque Pathomorphology: fibrous plaques rise above the surface of the vessel, lead to deterioration of blood flow and create local conditions for the formation of blood clots. In the small vessels of the heart, kidneys, and intestines, the presence of plaques in the intima of the feeding arteries leads to a deterioration in the blood circulation of the tissues, dystrophic and atrophic changes in these organs. Cholesterol crystals Blood vessels





    4. Stage of atheromatosis. necrosis of tissue in the center of the plaque Pathomorphology: necrosis of the center of the plaque. As a result of the destruction of vasa vasorum, intramural hematomas can occur. Tissue detritus in the center of the plaque consists of cholesterol crystals, xanthoma cells, and fragments of destroyed vessel structures.






    5. Stage of formation of atheromatous ulcers. An ulcer forms at the site of the atherosclerotic plaque. Pathomorphology: the plaque cover can open and cause tissue or fat embolism (fatty contents enter the lumen of the vessel, which causes blood clotting and thrombosis). Often, parietal thrombi form at the edge of an atheromatous ulcer, creating a risk of developing thromboembolism.


    6. Stage of atherocalcinosis. Over time, dystrophic calcification develops in an atheromatous ulcer—atherocalcinosis develops. With a dissecting table it is more often possible to detect all stages at the same time atherosclerotic changes in vessels - from spots and stripes to atherocalcinosis. This circumstance indicates a continuously progressive course of the process, with periods of exacerbation and remission.















































    1. Definition of the concept: A disease, the main symptom of which is a prolonged and persistent increase in blood pressure “primary” (idiopathic) - the cause is unknown; “secondary” or symptomatic hypertension, which is a manifestation of many diseases of the nervous system, endocrine systems, pathologies of the kidneys and blood vessels.


    2. Etiology hypertension. The etiology of hypertension is NOT FINALLY CLEAR Based on many observations, we can conclude that hypertension occurs as a result of prolonged neuropsychic stress in combination with a hereditary predisposition




    Crisis (malignant) course Fibrinoid necrosis of the afferent arteriole (PAS reaction) corrugation and destruction of the basement membrane of the endothelium; spasm of the arteriole; plasma impregnation or fibrinoid necrosis of its wall; thrombosis, sludge phenomenon. heart attacks and hemorrhages develop




    Classification of hypertension. Benign variant of the course 1. Preclinical stage. (functional) stage. An unstable increase in pressure, moderate hypertrophy of the muscle layer and elastic structures of arterioles and small arteries, spasm of arterioles, moderate hypertrophy of the left ventricle of the heart.


    Benign variant of the course The stage of widespread changes in arterioles. Plasma impregnation of arterioles and small arteries entails damage to endothelial cells, basement membrane, muscle cells and fibrous wall structures. Subsequently, hyalinosis of the arterioles or arteriolosclerosis occurs. Most often, arterioles and small arteries of the kidneys, brain, pancreas, intestines, retina, and adrenal capsules are exposed to plasma impregnation and hyalinosis. Elastosis, elastofibrosis and sclerosis of large arteries


    Classification of hypertension. Benign variant of the course 3. Stage of secondary changes in organs. Sclerosis and hyalinosis of small arteries and arterioles - decreased blood flow in organs 1. Hypertrophy of the left ventricle of the heart 2. Hemorrhagic cerebral infarction 3. Primary wrinkled kidneys