REVIEW FOR EXAM #3 FSN 420

REVIEW FOR EXAM #3 1. Pathogenesis of atherosclerosis­know the specific steps and the changes that take place in the endothelium Pathogenesis: - Atherogenic stimuli (inflammation) or mechanical injury: cells express adhesion molecules and growth factors that lead to recruitment of leukocytes in inflammatory response to injury - Leukocytes adhere and migrate into vessel wall, localize sub­endothelially and develop foam cells - Foam cells release growth factors and cytokines that promote recruitment of SMC and stimulate neointimal proliferation: lipid continues to accumulate and support endothelial dysfunction - Once in the tissue, monocytes evolve into macrophages, ingest oxidized cholesterol and become foam cells, which form fatty streaks - Events promote development of lipid rich atheromatous lesion (atheroma) - Atheromas can rupture forming a thronus, attacking platelets, activating clotting and - Thrombosis is initiated and ascade of events triggers fibro­proliferative lesin and luminal narrowing - Calcification occurs, forming deposits within vascular smooth muscular layer - Atherothrombossi: complex disease where rupture of high risk vulnerable plaques and atherosclerotic lesion disruption s cause thrombus formation - Leading cause of unstable angina, acute MI and sudden cardia death Changes in the endothelium: ASCVD involves the accumulation of plaque within the walls of the arteries. It starts with injury to the endothelial cells with an associated inflammatory response involving phagocytes and monocytes. Once in the tissue, monocytes evolve into macrophages that ingest oxidized cholesterol and become foam cells and then fatty streaks in these vessels. Intracellular microcalci­ fication occurs, forming deposits within the vascular smooth muscle cells of the surrounding muscular layer. A protective fibrin layer (atheroma) forms between the fatty deposits and the artery lining. Atheromas produce enzymes that cause the artery to enlarge over time, thus compensating for the narrowing caused by the plaque. This “remodeling” of the shape and size of the blood vessel may result in an aneurysm. Atheromas can rupture or break off, forming a thrombus (blood clot), where they attract blood platelets and activate the clotting system in the body. This response can result in a block­ age and restricted blood flow. Etiology: Smoking, obesitt, hypertension, elevated LDL cholesterol , stress, diabetes, inacitivy which lead to accumulation of plaque production of less ntric oide, oxidized LDL cholesterol taken up by macrophages, formation of foam clel snad fatty streaks Pathophysiology elevated LDL cholterol, elevated serum TG, c­reactive protein, low HDL cholesterol Nutrion managent: DASH, Mediterranean diet pattiern, weight reduction. 2. Characteristics of the metabolic syndrome and medical nutrition therapy Def: The metabolic syndrome is a combination of metabolic disorders, such as dyslipidemia, hypertension, impaired glucose tolerance, compensatory hyperinsulinemia and the tendency to develop fat around the abdomen. Individuals with the metabolic syndrome are at high risk for atherosclerosis and, consequently, cardiovascular disease. Some of the characteristics of Metabolic syndrome a. increased calories weight gain b. insulin resistance c. carrying more weight increased blood pressure, hypertension d. weight gain: hyperlipidemia. Some of the characteristics of Metabolic syndrome e. increased calories weight gain f. insulin resistance g. carrying more weight increased blood pressure, hypertension h. weight gain: hyperlipidemia. ATP III GUIDELINES: benefit beyond LDL­ lowering: the metabolic syndrome as a secondary target of therapy Benefit Beyond LDL lowering: the metabolic syndrome as a secondary target of therapy - General Features of the metabolic syndrome 1. Abdominal obesity 2. Atherogenic dyslipidemia: elevated triglycerides, small LDL particles, low HDL cholesterol 3. Raised blood pressure 4. Insulin resistance ( glucose intolerance) 5. Proinflammatory state Metabolic Syndrome Causes: Acquires causes: overweight and obesity; physical inactivity; high carbohydrate diets (> 60% of energy intake) in some persons - Genetic causes: Metabolic Syndrome Criteria or Diagnosis of the Metabolic Syndrome - Obesity: wait circumference - Men > 102 cm (> 40 in); men > 88 cm (> 35in) - Triglicerides: > or eq 50 mg/dl Cholesterol: men < 40, < 50 women Blood pressure > 130 and glucoe > 100 m ATP III Guidelines; Therapeutic lifestyle changes (TLC) New Features of ATP III: New strategies for promoting adherence; In both: TLC and drug therapy More intensive lifestyle intervention (therapeutic lifestyle changes = TLC) - Theraupetic diet lowers saturated fat and cholesterol intakes to levels of previous step II - Adds dietary iptions to enhance LDL lowering: Pans stanols/sterols (2 g/d); viscous (soluble) dibe (10­25 g/d) - Increased emphasis on weight management and physical activity Stanols/Sterols; binders of cholesterol, but also binds to fat soluble vitamins. - Isolated from soybean or pien tree oil - Lower blood cholesterol - Esterified and amade in margarine - 2­3 grams/day lowers cholesterol by 9­20%; inhibits absorption of dietary cholesterol - esters lower B­carotene and a tocopherol and lycopene MNT: Usually the daily energy intake consists of 30% fat, but no more than 10% of these calories should come from saturated (animal) fat