DYSLIPIDEMIA.

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Presentation transcript:

DYSLIPIDEMIA

Objectives At the end of this lecture you must be able to: Define different types of lipoprotein and recognize their functions. State the pathophysiology of atherosclerosis. Identify the primary and secondary causes of hyperlipidemia. Classify hyperlipoproteinemia. Determine when to check lipids and their goals. Outline the treatment lines of hyperlipidemia. List the main antihyperlipidemic agents.

Introduction

Definitions Lipids circulate in plasma as lipoproteins. Chylomicrons transport fats from the intestinal mucosa to the liver. In the liver, the chylomicrons release triglycerides and some cholesterol and become low-density lipoproteins (LDL). LDL then carries fat and cholesterol to the body’s cells. High-density lipoproteins (HDL) carry fat and cholesterol back to the liver for excretion.

HDL metabolism and reverse cholesterol transport

When oxidized LDL cholesterol gets high, it provokes inflammatory response, so monocytes recruited & transformed into macrophages resulting in cholesterol laden foam cell accumulation, which are beginning of arterial fatty streaks, then atheroma formation occurs, which causes atherosclerosis. HDL cholesterol is able to go and remove cholesterol from the atheroma. Atherogenic cholesterol → LDL, VLDL, IDL. VLDL= TG/5

Atherosclerosis Hyperlipidemia Hyperlipoproteinemia: abnormally increased plasma lipoproteins- one of the risk factor for atherosclerosis. Hyperlipemia: increased level of TG.

Hyperlipoproteinemia Fredrickson Classification Lipoprotein Elevation Synonyms Type Chylomicrons ''Primary hyperlipoproteinemia'', or ''Familial hyperchylomicronemia'' I (rare) LDL ''Polygenic or Familial hypercholesterolemia'‘ IIa LDL+VLDL ''Combined hyperlipidemia'' IIb Chylomicrons+IDL ''Familial dysbetalipoproteinemia'' III (rare) VLDL ''Familial hyperlipemia'' IV VLDL+ Chylomicrons ''Endogenous hypertriglyceridemia'' V (rare)

Hereditary Causes of Hyperlipidemia Caused by Known Single Gene Mutations Familial Hypercholesterolemia: Occurs in 1 in 500 individuals/ AD. Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life. High risk for atherosclerosis, tendon xanthomas and xanthelasmas of eyes, CHD Familial Combined Hyperlipidemia: Autosomal dominant. Increased secretions of LDL& VLDLs. High risk for atherosclerosis, no xanthomas. Dysbetalipoproteinemia: Affects 1 in 10,000 A binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL). Increased risk for atherosclerosis, palmar xanthomas, CHD, PVD.

Secondary Causes of Hyperlipidemia Hypothyroidism (high LDL) NS (high LDL) Cholestasis (high LDL) Obesity (high TG) DM type 2 (high TG & chylomicrons) Pregnancy (high TG) Sepsis (high TG) Stress Reduced HDL: smoking, DM2, obesity, malnutrition, B- blockers Acute hepatitis (high TG) Drugs (thiazide, steroids, B- blockers, cyclosporine, protease inhibitors). MM, lymphoma (high TG) Glycogen storage disease (high TG). Alcohol, interferon, estrogen, thiazide, steroid (high TG). Acromegaly, renal failure (high TG).

Checking lipids Nonfasting lipid panel Measures HDL and total cholesterol. Fasting lipid panel Measures HDL, total cholesterol and TG. LDL cholesterol is calculated: LDL = total cholesterol – (HDL + TG/5)

When to check lipid panel? Adult Treatment Panel (ATP III) of the National Cholesterol Education Program (NCEP): Beginning at age 20: obtain a fasting (9 to 12 hour) serum lipid profile consisting of total cholesterol, LDL, HDL and triglycerides. Repeat testing every 5 years for acceptable values. United States Preventative Services Task Force: Women aged 45 years and older, and men ages 35 years and older undergo screening with a total and HDL cholesterol every 5 years. If total cholesterol > 200 or HDL <40, then a fasting panel should be obtained. Cholesterol screening should begin at 20 years in patients with a history of multiple CV risk factors, DM, or family history of either elevated cholesterol levels or premature CVD.

Goals for Lipids LDL < 100 →Optimal 100-129 → Near optimal 130-159 → Borderline 160-189→ High ≥ 190 → Very High Total Cholesterol < 200 → Desirable 200-239 → Borderline ≥240 → High HDL < 40 → Low ≥ 60 → High Serum TG < 150 → normal 150-199 → Borderline 200-499 → High ≥ 500 → Very High

Determining Cholesterol Goal (LDL!) Look at JNC 7 Risk Factors. Cigarette smoking Hypertension (BP ≥140/90 or on treatment) Low HDL cholesterol (< 40 mg/dL) Family History of premature coronary heart disease (CHD) (CHD in first-degree male relative <55 or CHD in first-degree female relative < 65) Age (men ≥ 45, women ≥ 55)

LDL Goals 0-1 Risk Factors: LDL goal is 160 If LDL ≥ 160: Initiate TLC (therapeutic lifestyle changes). If LDL ≥ 190: Initiate pharmaceutical treatment. 2 + Risk Factors: LDL goal is 130 If LDL ≥ 130: Initiate TLC If LDL ≥ 160: Initiate pharmaceutical treatment CHD or CHD Risk Equivalent LDL goal is 100 (or 70) If LDL ≥ 100: Initiate TLC and pharmaceutical treatment

Treatment of Hyperlipidemia Therapeutic Lifestyle Changes (TLC): Restricted total fat, saturated fats, cholesterol intake. Moderate increase in polyunsaturated fat. Increase soluble fiber intake. Exercise: moderate intensity 30min/ day most days. Weight reduction ( initial goal of 10%) if needed. Smoking cessation. Treat HTN.

Dietary sources of Cholesterol Type of Fat Main Source Effect on Cholesterol levels Monounsaturated Olives, olive oil, canola oil, peanut oil, cashews, almonds, peanuts and most other nuts; avocados Lowers LDL, Raises HDL Polyunsaturated Corn, soybean, cottonseed oil; fish Saturated Whole milk, butter, cheese, and ice cream; red meat; chocolate; coconuts, coconut milk, coconut oil , egg yolks, chicken skin Raises both LDL and HDL Trans Most margarines; partially hydrogenated vegetable oil; deep-fried chips; many fast foods; most commercial baked goods Raises LDL

Most patients should receive 3 m TLC trial before starting drugs unless very high risk. If unable to reach goals with TLC alone choose lipid- lowering drugs based on lipoprotein disorder. Combination therapy may be necessary.

Medications for Hyperlipidemia Drug Class Agents Effects (% of change) Side Effects HMG CoA reductase inhibitors Lovastatin 20-80mg Pravastatin 40- 80mg Atrovastatin 10-80mg LDL,  TG,  HDL Myopathy, increased liver enzymes, rhabdomyolysis Cholesterol absorption inhibitor Ezetimibe 10 mg/d LDL,  HDL Triglyceride Headache, GI distress Nicotinic Acid Niacin 100- 1000mgtid ( LDL&VLDL synthesis)  Triglyceride Flushing, Hyperglycemia, Hyperuricemia, GI distress, hepatotoxicity Fibric Acids ( VLDL synthesis) Gemfibrozil 600mg bid Fenofibrate 145mg qd Clofibrate LDL, HDL Dyspepsia, gallstones, myopathy Bile Acid sequestrant Cholestyramine 4-30 g /d Colestipol 5-40 g/d LDL,  VLDL, GI distress, constipation, decreased absorption of fat soluble vit. and other drugs( digoxin,thyroxin, warfarin)

Omega 3 Fatty Acids Diet rich in omega 3 FA (oil fish) decrease TC, TG, increase HDL & decrease CV events. FDA approved as dietary adjunct for very high TG levels ( > 500 mg/ dl). < 3g daily is safe. Adverse effects: thrombocytopenia, abnormal LFT, worsening glycemic control, GI disturbance.

Hypertriglyceridemia Associated with lipoprotein types I, III, IV, V. Exclude primary disorders. TLC: - achieve desirable body weight. - diet low in saturated fat, cholesterol. - regular exercise. - smoking cessation. - alcohol restriction.

Borderline- high TG+ CHD risk factors: - FH of premature CHD. - concomitant LDL elevation or low HDL. - genetic forms associated with CHD (familial dysbetalipoproteinemia and familial combined hyperlipidemia - consider initiation of niacin. Alternative therapies: - gemfibrozil, statins, fish oil, fibrates.

Very high TG (> 500 mg/ dL) associated with pancreatitis. Genetic form often coexist with other causes like DM. Medications: - gemfibrozil: preferred in diabetics. - niacin. - higher potency statins. - fenofibrate.

Low HDL- C Strong CHD risk predictor. Causes: - DM type 2. - physical inactivity. - insulin resistance. - cigarette smoking. - very high carbohydrate intake. Treatment: TLC, drugs ( fibric acid derivatives, niacin)

a. What is the goal LDL in this woman? A 55-year-old woman without symptoms of CAD seeks assessment for routine health maintenance. Her BP is 135/85 mm Hg. She does not smoke or have diabetes and has been postmenopausal for 3 years. Her BMI is 24. The patient has no FH of premature CAD. Lipoprotein analysis shows: Total cholesterol = 240 mg/dL HDL = 55 mg/dL TG = 85 mg/dL LDL = 180 mg/dL. a. What is the goal LDL in this woman? b. What would you do if exercise/diet change do not improve cholesterol after 3 months?