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Hyperlipidemia

Mahesh Moolani, M.D. Diplomat American Board Of Internal Medicine and Lipidology. What’s The Big FAT Deal?. Hyperlipidemia. CHOLESTEROL. A soft waxy substance found among lipids (fats) in the bloodstream and all cells Needed for digesting fats, making hormones, building cell walls

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Hyperlipidemia

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  1. Mahesh Moolani, M.D. Diplomat American Board Of Internal Medicine and Lipidology What’s The BigFATDeal? Hyperlipidemia

  2. CHOLESTEROL • A soft waxy substance found among lipids (fats) in the bloodstream and all cells • Needed for digesting fats, making hormones, building cell walls • Carried in particles called lipoproteins that act as transport vehicles delivering cholesterol to various body tissues to be used, stored or excreted • Excess circulating cholesterol can lead to plaque formation- Atherosclerosis

  3. HYPERLIPIDEMIA OR DYSLIPIDEMIA(A consequence of abnormal lipoprotein metabolism) • Elevated Total Cholesterol (TC) • Elevated Low-density lipoproteins (LDL) • Elevated triglycerides (TG) • Decreased High-density lipoproteins (HDL)

  4. The story of lipids • 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.

  5. The story of lipids (cont.) • When oxidized LDL cholesterol gets high, atheroma formation in the walls of arteries occurs, which causes atherosclerosis. • HDL cholesterol is able to go and remove cholesterol from the atheroma. • Atherogenic cholesterol → LDL, VLDL, IDL

  6. Types of Cholesterol LDL-(“bad” cholesterol) The major cholesterol carrier in the blood. Excess most likely to lead to plaque formation. Goal: LOW HDL-(“good” cholesterol) Transports cholesterol away from arteries and back to the liver to be eliminated. Removes excess cholesterol from plaques, slowing growth. Goal: HIGH

  7. TYPES (CONT.) • Triglycerides-the chemical form in which most fat exists in foods as well as in the body. Present in blood plasma and together with cholesterol, form the plasma lipids. Made in the body from other energy sources like carbohydrates. Calories ingested in a meal and not immediately used by tissues are converted to triglycerides..

  8. PRIMARY DYSLIPIDEMIA ETIOLOGY • SINGLE OR MULTIPLE GENE MUTATION –RESULTING IN DISTURBANCE OF LDL, HDL AND TRIGYLCERIDE, PRODUCTION OR CLEARANCE. • Should be suspected in patients with • premature heart disease • family hxof atherosclerotic dx. • Or serum cholesterol level >240mg/dl. • Physical signs of hyperlipidemia.

  9. Hereditary Causes of Hyperlipidemia • Familial Hypercholesterolemia • Occurs in 1 in 500 individuals • Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life • High risk for atherosclerosis, tendon xanthomas (75% of patients), tuberous xanthomas and xanthelasmas of eyes. • Familial Combined Hyperlipidemia • Increased secretions of VLDLs • Dysbetalipoproteinemia • Affects 1 in 10,000 • Increased risk for atherosclerosis, peripheral vascular disease • Tuberous xanthomas, striae palmaris

  10. Diet Hypothyroidism Nephrotic syndrome Anorexia nervosa Obstructive liver disease Obesity Diabetes mellitus Pregnancy Obstructive liver disease Acute heaptitis Systemic lupus erythematousus AIDS (protease inhibitors) Causes of SECONDARY Hyperlipidemia

  11. SECONDARY DYSLIPIDEMIA (Most adult cases of dyslipidemia are secondary in nature in western civilizations) • Sedentary lifestyle • Excessive consumption of cholesterol – saturated fats and trans-fatty acids.

  12. Specific Dyslipidemias: Very High LDL (> 190mg/dl) Causes and Diagnosis • Genetic disorders Monogenic familial hypercholesterolemia Familial defective apolipoprotein B-100 (Apo B) Polygenic hypercholesterolemia • Family testing to detect affected relatives

  13. Dietary sources of Cholesterol

  14. Why Do We Care? According to the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Cholesterol in Adults (NCEP ATP-III): High LDL levels are a leading cause of coronary heart disease (CHD) and should be the main target of any cholesterol lowering regimen

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

  16. When to check lipid panel • Two different Recommendations • 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

  17. ATP III Lipid and Lipoprotein Classification LDL Cholesterol (mg/dl) HDL Cholesterol (mg/dl) <100 Optimal < 40 Low 100-129 Near/Above Optimal > 60 High (Desirable) 130-159 Borderline High 160-189 High >190 Very High Categories of Risk that Modify LDL Goals CHD and CHD risk equivalents <100 Multiple (2+) risk factors <130 Zero to one risk factor <160

  18. Major Risk Factors For CHD That Modify LDL Goals Cigarette smoking Hypertension (BP >140/90 or on BP med) Low HDL cholesterol (<40mg/dl) Family Hx premature CHD • CHD in male 1st degree relative <55 years old • CHD in female 1st degree relative <65 years old Age (men >45 yrs. women >55 yrs) • HDL >60 counts as a “negative” risk factor. It’s presence removes one risk factor from the total count

  19. Risk Assessment for CHD Diabetes regarded as a CHD equivalent For patients with multiple (2+) risk factors -Perform 10 year risk assessment For patients with 0-1 risk factor -Most have 10 year risk assessment <10%; risk assessment scoring unnecessary

  20. Current ATP III Guidelines for Treating LDL Cholesterol

  21. A Model of Steps in Therapeutic Lifestyle Changes (TLC) Visit 1 Begin TLC Visit 2 (6 wks) Eval. LDL response Intensify Tx if not to goal Visit 3 (6 wks) Eval LDL response Consider adding Rx if not to goal Visit N Monitor adherence to TLC Q4-6 mos • Emphasize reduction in saturated fat & chol. • Encourage moderate Physical activity • Consider referral to dietician • Reinforce dietary recommendations • Consider adding plant stanols/sterols • Increase fiber intake • Consider dietician • Evaluate for Metabolic syndrome • Intensify wt mgmt & physical activity • Consider dietician

  22. Nutrient Recommendations of TLC Diet NutrientRecommended Intake • Saturated fat < 7% of total calories • Polyunsaturated fat Up to 10% of total calories • Monounsaturated fat Up to 20% of total calories • Total fat 25-30% of total calories • Carbohydrates 50-60% of total calories • Fiber 20-30 grams/day • Protein Approx. 15% of total calories • Cholesterol <200 mg/day • Total calories Balance energy intake and expenditure to maintain desirable body weight/ prevent weight gain

  23. Food Pyramid

  24. Medications for Hyperlipidemia

  25. Specific Dyslipidemias: Low HDL Causes of Low HDL (<40 mg/dl) • Elevated triglycerides • Overweight and obesity • Physical Inactivity • Type 2 diabetes • Cigarette smoking • Very high carb. intakes (>60% energy) • Medications (some beta blockers, anabolic steroids, progestational agents)

  26. Specific Dyslipidemias: Elevated Triglycerides Classification of Serum Triglycerides Normal <150 mg/dl Borderline High 150-199 mg/dl High 200-499mg/dl Very High >500 mg/dl

  27. Specific Dyslipidemias: Elevated Triglycerides Causes of Elevated Triglycerides • Obesity and overweight • Physical Inactivity • Cigarette smoking • Excess alcohol intake • High carb. diets • Several diseases (Type 2 DM, chronic renal failure, nephrotic syndrome • Medications (corticosteroids, estrogens, retinoids, higher doses of beta blockers

  28. Specific Dyslipidemias: Elevated Triglycerides Management of Very High Triglycerides (>500 mg/dl) • Goal of therapy: Prevent acute pancreatitis • Very low fat diets (< 15% of caloric intake) • Triglyceride-lowering drug usually required (fibrate or nicotinic acid) • Reduce triglycerides before lowering LDL

  29. Lipid Lowering Drugs HMG-CoA Reductase Inhibitors (Statins) • Partially block an enzyme necessary for formation of cholesterol • Speed removal of LDL from blood • 18%-60% reduction in LDL • Most effective at lowering LDL; esp. HS dosing • Liver enzymes MUST be monitored. Check baseline, 3mos., then semi-annually (D/C if > 3x normal limits) • Side effects: Myalgias (D/C if total CK >10x normal), rhabdomyolysis • Metabolized by CP450 (watch for drug interactions)

  30. Lipid Lowering Drugs Bile Acid Sequestrants • Convert cholesterol to bile acids • Bind bile acids and prevent reabsorption in the gut • May increase triglyceride levels • Most common side effects: GI-constipation • Alternative for statins

  31. Lipid Lowering Drugs Cholesterol Absorption Inhibitor: Zetia • Monotherapy or in combination with statin • Reduces LDL number : esp. Lp(a) Lipid-Regulating Agent: Omega 3 acid ethyl esters (Lovaza) • Omega 3 Fish oil (salmon, herring, mackerel, swordfish, albacore tuna, sardines, lake trout) • Only FDA approved supplement for tx of dyslipidemias • Decreases hepatic production of TG and VLDL • Increases LDL size to large buoyant particles

  32. Lipid Lowering Drugs Nicotinic Acid/Niacin • Reduces production and release of LDL • Effective in reduction of triglycerides (<400mg/dl) • Increases HDL • Very effective in increasing LDL particle size • Monitor liver enzymes and glucose • Most common side effect: FLUSHING (take ASA/ibuprofen 30 min. prior and take with light snack). Decreased with time released formulas (Niaspan)

  33. Lipid Lowering Drugs Fibric Acid Derivatives/Fibrates • Very effective in reducing triglycerides (>400) • Increase HDL • Containdications: Gallbladder disease, hepatic disease, renal dysfunction • Increase LDL particle size but not quantity • Caution with statins

  34. Case Study 1 35 YO male, a police officer. 5’11’’, weight=258 (BMI=35, obese) Hx: hypertension, anxiety. Has taken testosterone supplements in past, now uses “body building” shakes. Family Hx: Father, paternal grandfather-DM Labs: FBS=79, TSH normal

  35. Case Study 1 Visit 1 Visit 2 Visit 3 TC= 167 164 158 TG=539 288 260 HDL= 18 24 28 LDL= ? 95 88 Tricor started Niaspan Levaza (intolerant)

  36. Case Study 2 39 YO male (hasn’t been in for 2 years) c/o frequent urination, excessive thirst, blurred vision. Hx: Mod. Obesity, BMI= 33 Family Hx: Mother DM Meds: None Non-fasting Accucheck= 297 (3 hrs PP)

  37. Case Study 2

  38. Case Study 3 62 YO Female with CHD s/p CABG wanted me to manage lipids. Also has Hypertension. Meds: Plavix, Atenolol, lisinopril, Atorvastatin (stopped by pt.-myalgias) Current labs: TC= 248 Trig= 144 HDL= 41 LDL= 156

  39. Case Study 3 • Changed atenolol to Coreg • Started Pravachol 20mg • Disease management/diet counseling • Resume walking 3-4 days/week • Repeat labs: TC=190 Increase Pravachol …178 Trig= 130 to 40mg …128 HDL= 39 …41 LDL= 112 …98

  40. Framingham Risk Prediction Score • 47 YO Female • Labs: TC= 178 Trig= 133 LDL= 110 HDL= 35 • BP: 162/98 • Hx: Smoker, non-diabetic What is 10 Year CHD Risk?

  41. Framingham Risk Prediction Score • 47 YO Female • Labs: TC= 178 Trig= 133 LDL= 110 HDL= 35 • BP: 162/98 • Hx: Smoker, non-diabetic What is 10 Year CHD Risk? 10% Compared to average of 5% for her age group

  42. Treatment of Dyslipidemias(Medication Comparison Chart) Which Medication(s) slows coronary athersclerosis, lowers LDL, increases HDL but has no effect on triglycerides?

  43. Treatment of Dyslipidemias(Medication Comparison Chart) Which Medication(s) slows coronary athersclerosis, lowers LDL, increases HDL but has no effect on triglycerides? Mevacor

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