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ENH 220 (3)

Coronary Artery Disease/ Myocardial Infarction and Drug therapies

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Environmental Health
ENH 220
Connie Barbour

CAD- week 6 –maryan’s personal study notes Chapter 36 – Coronary Artery Disease - Coronary artery disease (CAD) is a type of blood vessel disorder that is included in the general category of atherosclerosis; it may affect the heart’s arteries and produce various pathophysiological effects ESP the reduced flow of oxygen and nutrients to the myocardium. -cardiovascular disease is the major cause of death in Canada accounting for 29% of all deaths - Patients with CAD can be asymptomatic or develop chronic stable angina  Unstable angina and myocardial infarction (MI_ are more serious manifestations of CAD and are termed acute coronary syndrome (ACS)  Cardiovascular disease is the most common reason for hospitalization in Canada -Atherosclerosis: a major cause of CAD; is the hardening of the arteries; and is characterized by a focal deposit of cholesterol and lipids primiarily within the intimal wall of the arteryderived from 2 Greek words: athere, meaning “fatty mush,” and skleros, meaning “hard” can occur anywhere in the body, most often happens in the coronary arteries [arteriosclerotic heart disease (ASHD), cardiovascular heard disease (CVHD), ischemic heart disease (IHD) and coronary heart disease (CHD)]  inflammation and endothelial injury play a central role in the development of atherosclerosis -Intact endothelium is more than a simple barrier b/w the vessel wall and the lumen of the vessel  normally it is nonreactive to platelets and leukocytes as well as coagulation, finrinolytic, and complement factors it can be injured as a result of tobacco use, hyperlipidemia, hypertension, diabetes, hyperhomocysteinemia, and infection -C-protein (CRP) which is produced by the liver, is a nonspecific marker of inflammation the level of CRP rises with systemic inflammation and is increased in many patients with CAD chronic elevations of CRP are associated with unstable plaques and oxidation of low-density lipoprotein (LDL) cholesterol, leading to increased uptake by the macrophages in the lining macrophages -CAD is a progressive disease and takes many years to develop  when it becomes symptomatic, the disease process is usually well-developedstages of development in atherosclerosis are: a)fatty streak, b)fibrous plaque resulting from smooth muscle cell proliferation and c)complicated lesion  Fatty Streaks: the earliest lesions of atherosclerosis, are characterized by lipid-filled smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow tinge appears treatment that lowers LDL cholesterol may reverse this process Fibrous Plaque: is the beginning of progressive changes in the endothelium of the arterial wallusually endothelium repairs itself but not ppl w/CAD  LDLs and growth factors from platelets stimulate smooth muscle proliferation and thickening of the arterial wall; once injury occurs to the endothelium, lipoproteins transport cholesterol and other lipids in the arterial intima collegen covers CAD- week 6 –maryan’s personal study notes the fatty streak and forms a fibrous plaque with grey-whitish appearanceplaques can form on one portion of the artery or in a circular manner that involves the entire lumenborders can be smooth or irregular with rough, jagged edges result: narrowing of the vessel lumen and a reduction in blood flow to the distal tissues  Complicated Lesion: development of the atherosclerotic lesion is the most dangerous; as fibrous plaque grows, continued inflammation can result in plaque instability, ulceration and rupture once the integrity of the artery’s inner wall is compromised, platelets accumulate in large numbers and form a thrombuswhich adheres to the artery wallcauses further narrowing/total obstruction of the artery -Collateral Circulation some arterial anastomoses or connections exist within coronary circulation; 2 factors contribute to the growth and the extent of collateral circulation: 1) inherited predisposition to grow new blood vessels and b)the presence of chronic ischemia  atherosclerosis plaque offsets the development of collateral circulation except when CAD has a rapid onset or coronary spasm occurs, the amount of time is inadequate for collateral circulation development and the diminished arterial blood flow results in more sever ischemia or infarction Risk Factors for CAD - Tobacco use, elevated blood levels of apolipoprotein B or A-1, history of hypertension, DM, abdominal obesity, psychological factors, lack of fruit and vegtable intake, alcohol consumption and physical inactivity - Cardiac risk factors are catergorized as nonmodifable and modifiable × Non-modifiable risk factors: include age, gender, family history, ethinicty, and genetic inheritance × Modifiable risk factors- include elevated serum lipid levels, elevated BP, obesity, DM, metabolic syndrome, psychological states, and elevated homocysteine level Management of Ppl @ high risk - Once identified as high risk, preventative measures can be taken  risk factors like age, gender, ethnicity cannot be modified by the person can modify the risk of CAD by controlling or changing the additive effects of modifiable risk factors  should be encouraged to make changes in lifestyle, to reduce the risk of heart disease  the nurse can play a major role in the teaching health-promoting behaviours to the person @ risk for CAD Nutritional therapy: Omega-3 fatty acids reduce the risk associated with CAD Cholesterol-Lowering Drug therapy: a complete lipid profile should be obtained every 5 years beginning at age 20  treatment usually begins w/smoking cessation, dietary caloric restriction, decreased dietary fat, and cholesterol intake, increased physical activity and stress management Drugs that restrict lipoprotein production:  ‘statin drugs’ most widely used and studied lipid-lowering drugs  Atrovastatin, rosuvastatin, simvastatin = inhibit the synthesis of cholesterol in the liver by blocking CAD- week 6 –maryan’s personal study notes the 3-hyroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase  an unexplained result of the inhibition of cholesterol synthesis is an increase in heptatic LDL receptors  results in the liver’s ability to remove more LDL from the blodd and HDLs also increase slightly with the use of statins Acute Coronary Syndrome - Is associated with deterioration of an atherosclerotic plaque that was one stable - Occurs when myocardial ischemia is prolonged and not immediately reversible
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