Atherosclerosis pathogenetic mechanisms of development presentation. Presentation on the topic "atherosclerosis"


Atherosclerosis (from the Greek athere gruel and skleros hard) is a chronic disease characterized by the appearance in the walls of arteries of foci of lipid infiltration and proliferation of connective tissue with the formation of fibrous plaques that narrow the lumen of the vessel and disrupt the physiological functions of the affected arteries, which leads to organ and general circulatory disorders . The term atherosclerosis was introduced in 1904 by F. Marchand.


RISK FACTORS FOR ATHEROSCLEROSIS RISK FACTORS FOR ATHEROSCLEROSIS 1. dyslipidemia 2. age and older 3. male gender (smoking more, stress more often) 4. arterial hypertension - endothelial damage (increased angiotensin II, endothelin, etc.) 5. smoking - endothelial dysfunction, prothrombotic effect 6. impaired glucose tolerance, diabetes mellitus 7. excess body weight - “metabolic syndrome”, “deadly quartet” (obesity, insulin resistance, HLP and hypertension) 8. physical inactivity 9. “stress” type 10. family history of atherosclerosis 11. gout 12. poor nutrition






CLASSIFICATION OF ATHEROSCLEROSIS (A.L. MYASNIKOV, 1960) LOCALIZATION OF THE PROCESS 1. AORTA (diastolic murmur, dysphagia, hoarseness) 2. CORONARY ARTERIES 3. CEREBRAL ARTERIES 4. RENAL ARTERIES 5. MESENTERAL ARTERIES (weight loss angina abdominae) 6 PERIPHERAL ARTERIES – LERICHE SYNDROME






CLINIC OF ATHEROSCLEROSIS I. ATHEROSCLEROSIS OF THE THORACIC AORTA 1. aortalgia 2. difficulty swallowing 3. increase in the width of the vascular bundle (percussion) - 1-3 cm to the right 4. retrosternal pulsation 5. shortening of the second tone with a metallic tint, systolic murmur over the aorta 6. increase systolic blood pressure with normal diastolic blood pressure




III ATHEROSCLEROSIS OF THE MESENTERIAL ARTERIES 1. Sharp, burning pain in the abdomen (usually in the epigastrium, at the height of digestion, for 1-3 hours (“abdominal toad”) 2. The pain is relieved by nitroglycerin 3. The pain is accompanied by bloating, constipation, belching 4. Foul-smelling diarrhea 2-3 times a day 5. Reflex pain in the heart area, palpitations, irregularities, shortness of breath 6. Objectively: flatulence, decreased peristalsis, systolic murmur in the epigastrium 7. Gradual dehydration, exhaustion, decreased skin turgor


IV ATHEROSCLEROSIS OF THE RENAL ARTERIES 1. Vasorenal symptomatic arterial hypertension 2. Protein, red blood cells, casts in the urine 3. Progression of arterial hypertension 4. Above the renal arteries (in the middle of the distance between the navel and the xiphoid process on the left and right) systolic murmur


V OBLITERATING ATHEROSCLEROSIS OF THE ARTERIES OF THE LOWER LIMB 1. Subjective manifestations: weakness and increased fatigue of the lower leg muscles, chilliness and numbness of the legs, intermittent claudication syndrome 2. Pallor, coldness of the legs, trophic disorders 3. Weakening or absence of pulsation in the area of ​​the large arteries of the foot


EXAMINATION PROGRAM 1. General blood and urine analysis 2. Biochemical tests: triglycerides, cholesterol, pre- and -lipoproteins, transaminases, aldolase, total protein and protein fractions 3. ECG, echocardiography 4. Rheovasography of the lower extremities 5. X-ray of the aorta and heart


TREATMENT STRATEGY FOR ATHEROSCLEROSIS 1. Diet 10 table 2. Drug therapy 3. I lipid-lowering drugs statins - fluvastatin, lovastatin, etc. mg per day. 4. II anion exchange resins (sequestrants of bile acids) – Cholestramin or colestipol 5-12 g 2-3 times a day. 5. III nicotinic acid with 500 mg per day, gradually increasing the dose to 3 g per day in 1-3 doses 6. IV fibrates - gemfibrozil 7. Enterosorption, hemosorption, LDL-immunosorption 8. Surgical treatment




COMPLICATIONS OF ATHEROSCLEROSIS 1. ½ of all deaths and 1.3 deaths in persons aged 2. Angina pectoris 3. Myocardial infarction 4. Symptomatic vasorenal arterial hypertension 5. Heart failure 6. Stroke 7. Heart rhythm disturbances 8. Chronic renal failure 9 . Dissecting aortic aneurysm 10. Arterial thrombosis and embolism 11. Sudden death



CLASSIFICATION OF IHD (WHO, 1979) 1. PRIMARY CIRCULAR STRESS. 2. ANGINA: 2.1. Exercise angina pectoris: for the first time arising a stable progressive angina pectoris (spontaneous) Special form of angina pectoris (angina pectoris) 3. The myocardial myocardium is small -focal (intramural) large -focal (transmural). 4. POST-INFARCTION CARDIOSCLEROSIS. 5. HEART FAILURE. 6. HEART RHYTHM DISORDERS.


(VKSC AMS USSR, 1984) 1. Sudden cardiac death (primary cardiac arrest). 2. Angina Pectoris Angina pectoris: First-time angina Stable angina (indicating functional class from I to IV) Progressive angina (unstable) Spontaneous (special, variant, vasospastic) angina. 3. Myocardial infarction Large focal (transmural) Small focal. 4. Post-infarction cardiosclerosis. 5. Heart failure (indicating the form and stage). 6. Heart rhythm disturbances (indicating the form).


FUNCTIONAL CLASSES (FC) OF STABLE EFFECTIVE ANGINA (RESEARCH CENTER OF CARDIOLOGY, MOSCOW, 1984) FC-I – ATTACKS OCCUR DURING STRONG PHYSICAL ACTIVITY. FC-II – SEIZURES OCCUR WHEN WALKING AT A DISTANCE OF MORE THAN 500 M, WHEN RISING MORE THAN 1 FLOOR. FC-III – SEIZURES OCCUR WHEN WALKING AT A DISTANCE OF 100–500 m, WHEN RISING TO 1 FLOOR. FC-IV – SEIZURES OCCUR WITH MINOR PHYSICAL ACTIVITY, WALKING AT A DISTANCE OF UP TO 100 M.


CLASSIFICATION OF IHD (as amended by the IV Congress of Cardiologists of Uzbekistan, 2000) 1. Sudden coronary death (primary cardiac arrest) 2. Angina 2.1. Stable exertional angina I functional class II functional class III functional class IV functional class


2.2. Unstable angina New-onset angina. Progressive angina pectoris Angiospastic angina Early post-infarction angina Early postoperative angina Remember! Acute coronary syndrome – unstable angina, MI with and without Q.


3. Silent myocardial ischemia 4. Microvascular angina 5. Myocardial infarction With Q wave – QMI Without Q wave – NQMI 6. Post-infarction cardiosclerosis 7. Heart rhythm disturbance (indicating the form) 8. Heart failure (indicating the form and stage)




Stable angina 1. Diet - table Aspirin mg 3. Nitrates - nitrosorbide 40-60 mg/day. 4. Beta blockers: metaprolol mg/day 5. Calcium antagonists - verapamil mg/day, amlodipine 5 mg, diltiazem if it is impossible to prescribe beta blockers, 6. Capoten - in the presence of heart failure 7. Statins (lipostat, zocor mg/day) - for hypercholesterolemia 8. Surgical treatment GOAL OF TREATMENT Improving the patient's prognosis Improving the patient's quality of life Unstable angina 1. Aspirin 325 mg 2. Heparin or fraxiparin for 7 days, lengthening the clotting time by 1.5-2.5 times 3. Nitrates - nitrosorbide 60-80 mg/day 4. Beta blockers: propranolol mg/day

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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.


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.

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