Drugs For The Treatment And Prevention Of Atherosclerosis PDF

 for the Treatment Drugs and Prevention of Atherosclerosis Introduction > - characterized...

 for the Treatment Drugs and Prevention of Atherosclerosis Introduction > - characterized of the arteries the blood vessel lumen and blood flow by buildup plague in , narrowing limiting ↳ main cause of coronary artery disease - canad to heart failure lead to peripheral artery disease > - can disease carotid artery , , and chronic kidney disease drugs behavioural blood > - combo w/ have been utilized d to in change successfully cholesterol , triglycerides and their related lipoproteins The > - responsible Coronary Arteries for supplying Oxygenated blood to the heart Atherosclerosis fatty sludge infiltrates the coronary artery > - In a inner wall so that the narrowed , coronary artery will carry I boods accumulation of white blood cells (live dead) and lipids ↳ heart will receive O2 to function Leventually calcium will deposit In these plagues and cause e max stiffness capacity (like heart cope at rest but when hm ↑ during exercise) the heart ↳ can , doesn't get enough oxygen and the individual experiences angina pectoris (che Behavioural Risk Factors (L20 % overweight Obesity · · Cigarette smoking · Lack of exercise Hypertension s Lipoproteins compinesw/ transport fut protein > - that > - types of lipoproteins : largest, mabadattef a transports formed in > - "good" be it from arteries cholesterol away toliverwhereCholester a s intestine to a carry triglycerides acids's excreted ordietaryoriya density lipoproteins) densityy highdendya rhine) (low (very low against heart disease * HDL helps protect ↳ secreted by liver Cholesterol esters ↳ carry triglycerides for utilisation or storage from dietary carbohydrates  Hyperlipoproteinemias lipids/fate triglycerides blood disordere characterized by inability to break down body specifically cholesterol and > - in , from gene defect inhereted Mendelian fashion (may be in combo w/ · primary arises predictible : in environmental factors of secondary · aris as complications metabolic disturbances : more generalized of Inciting condition diabetes ↳ such as , hypothyroidism , Chronic ingestion large amounts of alcohol Link Between Cholestero and Heart Disease calculation of MDL/LDL ratio requires > - ↳ not sufficient look at cholesterd to only triglycerides associated > - also less cholesterol and Therapeutic Measures I saturated feet and to improve LDL blood cholesterd Behavioural changes Celimination of aggravating factore and institution of dietary changes · Drug therapy may also be needed · * deatials of therapy will depend on lipid analyses of blood ↳ drug of choice dependant on type of lipid causing issue (Cholesterol , LDL , triglycerides Drug Therapies for Hyperlipoproteinemia - lipid analysis must be done first on blood sample > - however , in general , the first line of treatment is stations ① Statins - Inhibit HMG-CoA in the liver ↳ Catalyses rate-limiting step in cholesterol biosynthesis from produced (d blood LDL) ↳ removed ensures more LDL is the body than w/ most effective druy class to lower LDL and cholestera levels especially In combination - , good diet + exersize (disease of Iliver ena b adverse effects muscles causing function) and mypathy improper : damage  ② Inhibitors of Stero Absorption (Ezetimibe) Inhibits for transporter absorption of cholesterd > - In G1 tract responsible and other sterols , I plasma levels in the bedy > - can also block reabsorption of bile salle which leads to conversion of cholester to bile salts in , - liver, sleral leda o wh stating Ezetimibe > - ex. ③ Fibric Acid Derivatives (Gemfibrozil) ↓ liver's d > - VLDL In plasma by 4 breakdown of triglycerides , & VLDL secretion by by breakdown of futty acids In adipose tissue therapeutic treatment of (triglycerides predominate & VLDL high use hypertriglyceridemia is > - = mmmm adverse effects rashes 21 upset hyperkalemia myopathy = , , , > - ex. Gemfibrozil ④ Bile Acid Binding Resins (ex. Cholestyramine mechanism of action : 1. In liver cholesterol is metabolized to bile acids bile acids of fate & reabsorbed 2. are excreted into SI did to in digestion most get from intestine 3. Bile acid binding resins (t charge) bind to bile acids in intestine , Inhibiting their reabsorbing enhancing their excretion ↳ enhanced cholestere to bile liver results in in d helps lower LDL-cholesterol 20 % by w ex. Cholestyramine adverse effects constipation bloating = + - protein in liver that regulates cholesterol metabolism ⑤ PCSK9 Inhibitor > - these drugs are monoclonal antibodies targeted against the paska protein act by 4 the livers ability to remove LDL cholesterol from the blood effective for I last ↓ drug > - resort mmm - compliance LDL levels > - given by Injection 2-4 weeks & & LDL levels by as much as 68-70 % every adverse effect= mild skin & Site of Injection &s upper tract Infections reactions respiratory > - limition = $$ ex. Alirocumab and Evolocumab