DYSLIPIDEMIA PHARMACOLOGY. University of Hawai i Hilo Pre- Nursing Program NURS 203 General Pharmacology Danita Narciso Pharm D
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1 DYSLIPIDEMIA PHARMACOLOGY University of Hawai i Hilo Pre- Nursing Program NURS 203 General Pharmacology Danita Narciso Pharm D 1
2 LEARNING OBJECTIVES Know normal cholesterol levels Understand what the role of LDL, HDL, and TGs are in the body 2
3 WHAT IS CHOLESTEROL? Cholesterol: A waxy fat-like substance that is found in all cells of the body Important in the synthesis of many endogenous substances. Normal serum total cholesterol <200 mg/dl The Good HDL The Bad LDL & The Triglycerides High density lipoprotein Carries cholesterol to the liver to prepare it for excretion from the body Should be >40 mg/dl Low density lipoprotein Carries cholesterol to the cells of the body Elevated levels leads to a build up in arteries Should be < 100 mg/dl Triglycerides a type of lipid/fat in the blood Comes from calories not used immediately, stored in fat cells Should be < 150 mg/dl 3
4 WHAT ARE THE SIGNS AN SYMPTOMS OF HIGH CHOLESTEROL? There are no symptoms of high cholesterol Lipid panel should be part of a regular check-up Elevated lipid panel increases risk of coronary heart disease (CHD) Cardiovascular Disease Risk Factors Hypertension Obesity (body mass index >30 kg/m2 ) Dyslipidemia Diabetes mellitus Cigarette smoking Physical inactivity Microalbuminuria, estimated glomerular filtration rate 55 for men, >65 for women) Family history of premature CVD (men age 4
5 CHOLESTEROL MOVEMENT AND LIPOPROTEINS Chylomicron Large particles that transport cholesterol from the diet/gi tract to the liver Cleared by lipoprotein lipase VLDL Large particles formed in the liver from endogenous cholesterol Shrink in size as lipoprotein lipase and hepatic lipase remove 5
6 CHOLESTEROL MOVEMENT AND LIPOPROTEINS LDL Carry the most cholesterol SD-LDL = too much lingering LDL HDL Transports lipid from periphery to liver where it is metabolized and excreted Represents apolipoproteins, help with binding to appropriate targets 6
7 CHOLESTEROL IN THE BODY Cholesterol Made in the liver Circulated in the blood TOO MUCH CHOLESTEROL 7
8 THIS IS WHAT HAPPENS Starts with damage to the endothelial cell in the wall of the artery Substances begin to enter the damaged area (including LDL) Chemical reactions lead to the oxidation of the cholesterol molecules Chemical messengers are sent from the damage site for immunologic cells to clean up Monocytes turn to macrophages that eat the cholesterol molecules Macrophages puff up convert to foam cells and begin to grow and turn to plaque The plaque grows and expands pushes into the lumen of the vessel Endothelial cells break off and cover and seal around the outside of the plaque (stable vs unstable) Vessel could be occluded Plaque could rupture 8
9 FACTS ABOUT CHOLESTEROL AND AMERICANS 31.7% US adults has high LDL What is considered high LDL? Less than half are receiving treatment. 1 in 3 of those adults actually has the condition under control. TOO MUCH CHOLESTEROL TOO MUCH CHOLESTEROL 9
10 STRATEGIES FOR TREATMENT Reduce the amount of dietary cholesterol Increase the clearance of cholesterol from the body 10
11 STRATEGIES FOR TREATMENT Reduce cholesterol absorption 1. Low fat/calorie diet and exercise 2. Low fat/calorie diet and exercise WITH drugs that reduce lipoprotein synthesis 3. Low fat/calorie diet and exercise WITH drugs that inhibit cholesterol absorption Increase cholesterol clearance 1. Exercise 2. Low fat/calorie diet and exercise WITH lipoprotein lipase support 3. Low fat/calorie diet and exercise WITH cholesterol receptor support 11
12 Effects on. Class LDL C HDL C TG Common ADRs HMG CoA reductase inhibitors (statins) 18% - 55% 5% - 15% 7% - 30% Myopathy Increased LFTs Niacin/nicotinic acid 2% - 25% 15% - 35% 20% - 50% Flushing, hyperglycemia, hyperuricemia/gout, upper GI upset, hepatotoxicity Fibric acids 15% - 30% 10% - 20% 20% - 50% Dyspepsia, gallstones, myopathy, unexplained non- CHD deaths in WHO study Bile acid sequestrants (resins) 15% - 30% 3% - 5% No change Gastrointestinal distress, constipation, decreased absorption of other drugs Azetidinones (usually as adjuncts, limited data as monotherapy) 16% - 20% 1% - 4% 5% - 6% Gastrointestinal distress, headache, joint pain Please see page 639 of your text for full reference. 12
13 13
14 STATINS MOA HMG CoA reductase inhibitor Upregulation of LDL receptor in the liver Base hits!!! Other Effects Anticancer effects Decrease inflammation Decrease coagulation Others Home run!!! 14
15 STATINS Uses: Indicated for hypercholesterolemia works on each type of cholesterol, greatest on LDL Statin selection: All work equally well. Have varying potencies. Statin selection Insurance coverage Cost Adverse effect profile Dosing: Taken orally prior to bed Heavy first pass metabolism LAS Lovastatin, atorvastatin, simvastatin (CYP 3A4) GPACMAN/PSPORCS Fluvastatin and rosuvastatin (CYP2C9) Amiodarone & verapamil increase the risk for myopathy 15
16 STATINS Adverse Drug Reactions: Teratogenic (pregnant, lactating, or might become pregnant no statin), not to be used in children under 16, liver toxicity (0.5%), rhabdomyolysis RHABDO Muscle pain/fatigue Cola urine Elevated creatinine kinase Monitoring Lipid panel CK LFTs 16
17 NIACIN Works great on triglycerides. Reduces VLDL which carries mostly TG 20% - 50% Works pretty good on HDL. Best medication we have for increasing HDL 15% - 35% Only modest decreases in LDL cholesterol 2% - 25% 17
18 NIACIN Uses: Hypertriglyceridemia, mixed hyperlipidemia, familial hypercholesterolemia Dosing: Start low and go slow. Titrate. The titration schedule is different if niacin is being combined with other lipid lowering agents: In combo with a BAR 500 mg once orally at bedtime, increase in 500 mg intervals every four week, mas of 2000 mg /day 250 mg immediate release daily, titrate every 4-7 days until at g daily in divided doses, if not adequate cholesterol lowering titrate every 2-4 weeks to 3 g daily in divided doses Extended release niacin is not to be substituted with equal doses of immediate release niacin WHY WHY WHY?????? 18
19 NIACIN ADRs Flushing Increased secretion of gastric acid CI in peptic ulcer Reduced glucose tolerance CI in insulin resistance Hepatotoxicity Hyperuricemia Monitoring Lipid panel LFTs Blood glucose Prothrombin time Signs and symptoms of jaundice Muscle pain 19
20 FIBRIC ACID Gemfibrozil & fenofibrate Uses: Hypertriglyceridemia MOA: Targets the PPAR alpha receptor located on the liver, kidney, heart, skeletal muscle, and adipose tissue. Binding of this receptor leads to an increase in LPL leads to an increase in fat breakdown. PPAR alpha also activates proteins that take up those cholesterol fragments and package them for disposal or enable them to be used by other cells ADRs: Increased LDL, weight gain, gallstones, myositis CI: Lovastatin & simvastatin co-administration Pregnancy & lactation: Used with extreme caution in pregnancy and not recommended for lactation Monitor: Lipid panel, LFTs, and CBC 20
21 BILE ACID RESIN (BAR) Colestipol, cholestryramine, colesevelam (naming scheme begin with col or chol) Use: Primarily used to reduce LDL cholesterol MOA: Bind to bile acids in the intestine to prevent reabsorption. Liver uses cholesterol to make more bile acids and upregulates cholesterol receptors to collect more cholesterol from the blood for this process. ADRs: Constipation, bloating, dry skin, abdominal cramping Drug interactions: Decrease the absorption of fat soluble vitamins, folic acid, iron, digoxin, thiazide diuretics, warfarin, thyroxine, etc. Pregnancy safe not absorbed Monitor: Lipid panel, drug levels if administered with medication that can have absorption altered 21
22 AZETIDINONES Ezetimibe Uses: Works well as an adjunct medication to statin therapy. Not used as monotherapy. MOA: Selective inhibitor of intestinal cholesterol reabsorption and reduced reabsorption of cholesterol secreted in the bile ADRs: Increased incidence of rhabdo (by itself for with statins), headache, GI upset Monitor: Lipid panel, CK?? 22
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