serum lipid abnormalities
DESCRIPTION
Hyperlipidemia is a common problem in the medical clinics. Almost 1 family member in this world has this problem. I am trying in these slides to introduce these abnormalities.At the end of this slideshow you will be able to:1. Know the different types of lipid abnormalities.2. Diagnose Hyperlipidemia.3. Screen for Hyperlipidemia.4. Manage abnormal lipid panels.I hope you'll find these slides helpful. Let me know if you have any questions.TRANSCRIPT
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Serum Lipid Serum Lipid AbnormalitiesAbnormalities
M Chadi Alraies, MDM Chadi Alraies, MDChief Medical ResidentChief Medical Resident
Case Western Reserve University / St. Vincent HospitalCase Western Reserve University / St. Vincent Hospital
Cleveland, OhioCleveland, Ohio
Saturday, December 20, 2007Saturday, December 20, 2007
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A quick look at the A quick look at the differential differential
diagnosis of Heart diagnosis of Heart MurmursMurmurs
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or or or or or or or
Intervention HOCM Aortic Stenosis Mitral Regurgitation
Valsalva IncreasedIncreased DecreasedDecreased Decreased Decreased or sameor same
Standing IncreasedIncreased IncreasedIncreased DecreasedDecreased
Handgrip or squatting
DecreasedDecreased DecreasedDecreased IncreasedIncreased
Supine position with legs elevated
DecreasedDecreased IncreasedIncreased No changeNo change
Exercise IncreasedIncreased IncreasedIncreased DecreasedDecreased
Amyl nitrite Markedly Markedly increasedincreased
IncreasedIncreased DecreasedDecreased
Iso-Proterenol
Markedly Markedly increasedincreased
IncreasedIncreased DecreasedDecreased
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Lipid Lipid abnormalitiesabnormalities
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TerminologyTerminology
Primary preventionPrimary prevention Secondary preventionSecondary prevention Lipoproteins.Lipoproteins. Apoproteins.Apoproteins.
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General considerationGeneral consideration
The two main lipids in blood are The two main lipids in blood are cholesterol and triglyceride. cholesterol and triglyceride.
Why lipids are deposited into the Why lipids are deposited into the walls of large and medium-sized walls of large and medium-sized arteries is not known. arteries is not known.
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LipoproteinsLipoproteins
Particles that have a hydrophobic Particles that have a hydrophobic core (TG/Cholesterol), core (TG/Cholesterol),
Surrounded by a hydrophilic Surrounded by a hydrophilic phospholipid outer layers which phospholipid outer layers which allows transport through the blood.allows transport through the blood.
LDL, VLDL, IDL, CHYLOMICRONS, LDL, VLDL, IDL, CHYLOMICRONS, HDLHDL
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ApoproteinsApoproteins
Small proteins.Small proteins. Surrounding Lipoproteins.Surrounding Lipoproteins. Helps lipoproteins:Helps lipoproteins:
Binding to receptors.Binding to receptors. Activating enzymes.Activating enzymes.
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LIPOPROTEINS & LIPOPROTEINS & ATHEROGENESISATHEROGENESIS
The higher the LDL, the greater the risk The higher the LDL, the greater the risk of CHD.of CHD.
The higher the HDL, the lower the risk The higher the HDL, the lower the risk of (CHD). of (CHD).
The mechanism of formation of The mechanism of formation of atherosclerotic plaques is not known. atherosclerotic plaques is not known.
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Lipid Fractions Lipid Fractions
In fasting serum…In fasting serum…
Most triglyceride is found in VLDL Most triglyceride is found in VLDL particles, which contain five times as particles, which contain five times as much triglyceride by weight as much triglyceride by weight as cholesterol. cholesterol.
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Lipid FractionsLipid Fractions
the LDL should always be estimated the LDL should always be estimated as the mean of at least two as the mean of at least two determinations…determinations…
Valid only if TG < 400 mg/dlValid only if TG < 400 mg/dl
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LipoproteinsLipoproteins
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Chylomicrons (I)Chylomicrons (I)
Large globules.Large globules. Apo (B48, CII, E)Apo (B48, CII, E) CII activates LPL (lipoprotein CII activates LPL (lipoprotein
lipase).lipase). LPL removes TG from chylomicrons.LPL removes TG from chylomicrons. Familial LPL deficiencyFamilial LPL deficiency Familial CII deficiency.Familial CII deficiency.
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VLDL (IV)VLDL (IV)
Apo (B100, CII, E)Apo (B100, CII, E) Smaller than chylomicronsSmaller than chylomicrons Contain more cholesterol than Contain more cholesterol than
chylomicrons.chylomicrons. Metabolized by LPL by means of CII.Metabolized by LPL by means of CII. Familial LPL deficiencyFamilial LPL deficiency Familial CII deficiency.Familial CII deficiency. FCHLFCHL
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IDL (III)IDL (III)
Apo B100, EApo B100, E VLDL remnant.VLDL remnant. ½ taken by liver. Strong affinity to ½ taken by liver. Strong affinity to
B100 & EB100 & E ½ stays in plasma and convert to ½ stays in plasma and convert to
LDL.LDL. Familial betadyslipoproteinemia.Familial betadyslipoproteinemia.
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LDL (IIA)LDL (IIA)
Apo B100…ONLY!Apo B100…ONLY! Formed from IDLFormed from IDL 2/3 binds to receptors & 1/3 2/3 binds to receptors & 1/3
scavenged.scavenged. Liver receptors have a weak affinity Liver receptors have a weak affinity
to B100.to B100. Familial hypercholesterolemia.Familial hypercholesterolemia. FCHLFCHL
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LDL receptors LDL receptors Down-regulated or decreased:Down-regulated or decreased:
High dietary cholesterol or saturated fat.High dietary cholesterol or saturated fat. AgeAge Familial hypercholesterolemia.Familial hypercholesterolemia.
Up-regulated or increased:Up-regulated or increased: Low dietary cholesterolLow dietary cholesterol EstrogenEstrogen ThyroxineThyroxine Acute illnessAcute illness Meds: statins and bile acid resins.Meds: statins and bile acid resins.
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HDLHDL
Apo (A1, A2, C)Apo (A1, A2, C) Protein and phospholipids.Protein and phospholipids. Very little cholesterol and TG Very little cholesterol and TG Scavenges the unesterified Scavenges the unesterified
cholesterol.cholesterol. Low HDL Low HDL low apo C (including low apo C (including
CII)CII)
increased VLDL and Chylomicrons.increased VLDL and Chylomicrons.
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Familial hyperlipidemia Familial hyperlipidemia syndromessyndromes
TypeType What is What is elevated?elevated?
DefectDefect NameName
II TGTG
(chylomicrons)(chylomicrons)LPL deficiencyLPL deficiency
CII deficiencyCII deficiencyFamilial LPL Familial LPL
deficiencydeficiency
Familial CII Familial CII deficiencydeficiency
IIAIIA CholesterolCholesterol
(LDL)(LDL)Decreased LDL receptorsDecreased LDL receptors
Apo B + VLDL overproductionApo B + VLDL overproductionFamilial Familial
hypercholesterolehypercholesterolemiamia
FCHLFCHL
IIBIIB TG + TG + CholesterolCholesterol
(LDL & VLDL)(LDL & VLDL)
Apo B + VLDL overproductionApo B + VLDL overproduction FCHLFCHL
IIIIII TG + TG + Cholesterol Cholesterol
(IDL)(IDL)
Abnormal apo E (E2/E2)Abnormal apo E (E2/E2) Familial Familial dysbetalipoproteidysbetalipoprotei
nemianemia
IVIV TGTG
(VLDL)(VLDL)LPL deficiencyLPL deficiency
CII deficiencyCII deficiency
Apo B + VLDL overproductionApo B + VLDL overproduction
Familial hyper TGFamilial hyper TG
FCHLFCHL
Familial CII Familial CII deficiencydeficiency
VV TG TG
Chylomicrons & Chylomicrons & VLDLVLDL
LPL deficiencyLPL deficiency
CII deficiencyCII deficiency
Apo B + VLDL overproductionApo B + VLDL overproduction
Familial LPL Familial LPL deficiencydeficiency
FCHLFCHL
Familial CII Familial CII deficiencydeficiency
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I + IV = V have isolated I + IV = V have isolated hypertriglyceridemiahypertriglyceridemia
IIa = cholesterol aloneIIa = cholesterol alone IIb and III = both cholesterol and IIb and III = both cholesterol and
TG.TG.
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Clinical findingsClinical findings
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Tendinous xanthomas: Achilles Tendinous xanthomas: Achilles xanthomas xanthomas
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Tendinous xanthomas: elbow Tendinous xanthomas: elbow xanthomas xanthomas
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Tendinous xanthomas: knuckle Tendinous xanthomas: knuckle xanthomas xanthomas
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Lipemia retinalisLipemia retinalis
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CLINICAL CLINICAL PRESENTATIONSPRESENTATIONS
No specific symptoms or signs.No specific symptoms or signs. Triglyceride level (>1000 mg/dL)Triglyceride level (>1000 mg/dL)
eruptive xanthomaseruptive xanthomas High LDL concentrations High LDL concentrations
TTendinous xanthomasendinous xanthomas on tendons of on tendons of (Achilles, patella, back of the hand).(Achilles, patella, back of the hand).
Triglyceride levels (above 2000 Triglyceride levels (above 2000 mg/dL):mg/dL): Lipemia retinalis.Lipemia retinalis.
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SECONDARY SECONDARY CONDITIONS CONDITIONS THAT AFFECT THAT AFFECT
LIPID LIPID METABOLISMMETABOLISM
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CauseCause Associated Lipid AbnormalityAssociated Lipid Abnormality
Obesity Increased triglycerides, decreased HDL cholesterol
Sedentary lifestyle Decreased HDL cholesterol
Diabetes mellitus Increased triglycerides, increased total cholesterol
Alcohol use Increased triglycerides, increased HDL cholesterol
Hypothyroidism Increased total cholesterol
Hyperthyroidism Decreased total cholesterol
Nephrotic syndrome Increased total cholesterol
Chronic renal insufficiency Increased total cholesterol, increased triglycerides
Hepatic disease (cirrhosis) Decreased total cholesterol
Obstructive liver disease Increased total cholesterol
Malignancy Decreased total cholesterol
Cushing's disease (or corticosteroid use) Increased total cholesterol
Oral contraceptives Increased triglycerides, increased total cholesterol
Diuretics Increased total cholesterol, increased triglycerides
Beta Blockers Increased total cholesterol, decreased HDL
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Therapeutic Effects of Lowering Therapeutic Effects of Lowering Cholesterol Cholesterol
Primary prevention is statistically Primary prevention is statistically significant and showed clinically significant and showed clinically important reductions in:important reductions in: Rates of myocardial infarctions, Rates of myocardial infarctions, New cases of angina, New cases of angina, Need for coronary artery bypass Need for coronary artery bypass
procedures. procedures. In general, decrease in In general, decrease in morbiditymorbidity..
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Primary prevention Primary prevention Pravastatin: West of Scotland Study.Pravastatin: West of Scotland Study. Lovastatin: AFCAPS/TexCAPS study.Lovastatin: AFCAPS/TexCAPS study. Atorvastatin: (ASCOT) study.Atorvastatin: (ASCOT) study.
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Secondary preventionSecondary prevention
1.1. Regression of atherosclerotic Regression of atherosclerotic plaques.plaques.
2.2. Reduces the progression of Reduces the progression of atherosclerosis in saphenous vein atherosclerosis in saphenous vein grafts.grafts.
3.3. Slow or reverse carotid artery Slow or reverse carotid artery atherosclerosis. atherosclerosis.
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SECONDARY CONDITIONS THAT SECONDARY CONDITIONS THAT AFFECT LIPID METABOLISMAFFECT LIPID METABOLISM
These are important for two reasons:These are important for two reasons: Abnormal lipid levels may be the Abnormal lipid levels may be the
presenting sign of some of these presenting sign of some of these conditions.conditions.
correction of the underlying condition correction of the underlying condition may obviate the need to treat an may obviate the need to treat an apparent lipid disorder. apparent lipid disorder.
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SCREENING FOR SCREENING FOR HIGH BLOOD HIGH BLOOD
CHOLESTEROLCHOLESTEROL
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Who should be screened for Who should be screened for high lipids?high lipids?
CHDCHD CHD risk equivalents:CHD risk equivalents:
1.1. Peripheral Peripheral arteryartery disease. disease.
2.2. AAAAAA
3.3. SymptomaticSymptomatic carotid artery disease carotid artery disease
4.4. Diabetes mellitusDiabetes mellitus
5.5. Multiple risk factors that confer a Multiple risk factors that confer a greater than 20% 10-year risk for greater than 20% 10-year risk for developing CHD!developing CHD!
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National Cholesterol Education National Cholesterol Education Program (NCEP):Program (NCEP): Screen all adults aged 20 years or older.Screen all adults aged 20 years or older.
USPSTF:USPSTF: Screen every 35 years in men and age 45 Screen every 35 years in men and age 45
years in women unless there are other years in women unless there are other risk factors for CHD.risk factors for CHD.
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Risk factors of coronary artery Risk factors of coronary artery diseasedisease
Age and gender Age and gender Men aged 45 years or older.Men aged 45 years or older. Women aged 55 years or olderWomen aged 55 years or older
A family history of premature CHD:A family history of premature CHD:1.1. MI or sudden cardiac death MI or sudden cardiac death
1.1. <55 years in a 1<55 years in a 1stst degree degree malemale relative. relative.
2.2. <65 years in a 1<65 years in a 1stst degree female relative. degree female relative.
2.2. Hypertension (whether treated or not.)Hypertension (whether treated or not.)
3.3. Current cigarette smoking (10 or more Current cigarette smoking (10 or more cigarettes per day).cigarettes per day).
4.4. HDL cholesterol (< 40 mg/dL). HDL cholesterol (< 40 mg/dL).
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10-year risk of developing CHD 10-year risk of developing CHD using Framingham projections using Framingham projections
of 10-year risk of 10-year risk Because risk factors alone are an Because risk factors alone are an
imprecise measure of CHD risk, imprecise measure of CHD risk, estimating the 10-year risk using estimating the 10-year risk using Framingham data is likely to be Framingham data is likely to be helpful even in patients with one or helpful even in patients with one or no risk factors. no risk factors.
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Screening in WomenScreening in Women
Low HDL is more important risk factor Low HDL is more important risk factor than a high LDL cholesterol in women.than a high LDL cholesterol in women.
Using estimates of 10-year CHD risk Using estimates of 10-year CHD risk may be particularly helpful in women.may be particularly helpful in women.
Women are less likely to benefit from Women are less likely to benefit from therapy unless their LDL cholesterol is therapy unless their LDL cholesterol is extremely high (greater than 190 extremely high (greater than 190 mg/dL).mg/dL).
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Screening in Older Screening in Older PatientsPatients
Patients age 75 years or older:Patients age 75 years or older: + CHD: LDL-lowering therapy can be + CHD: LDL-lowering therapy can be
continued. continued. No CHD: recommend screening and No CHD: recommend screening and
treatment.treatment. Decisions to discontinue therapy:Decisions to discontinue therapy:
Overall functional status.Overall functional status. Life expectancy.Life expectancy. Comorbidities.Comorbidities. Patient preference.Patient preference.
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TreatmentTreatment
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Goal of treatmentGoal of treatment
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Risk Category LDL Goal (mg/dL) LDL Level at Which to Initiate Lifestyle Changes
(mg/dL)
LDL Level at Which to Consider
Drug Therapy (mg/dL)
High risk: CHD or CHD risk equivalents (10-year risk > 20%)
< 100 100 100
Moderately high risk: 2+ risk factors
(10-year risk 10% to 20%)
< 130 130 130
Moderate risk: 2+ risk factors
(10-year risk < 10%)
< 130 130 160
Low risk: 0–1 risk factors
< 160 160 190
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Treatment of High LDL Treatment of High LDL Cholesterol Cholesterol
General measures:General measures: Quitting smoking: increase HDL & Quitting smoking: increase HDL &
lower LDL.lower LDL. Exercise (and weight loss) reduce the Exercise (and weight loss) reduce the
LDL increase the HDL. LDL increase the HDL. Modest alcohol use (1–2 ounces a day): Modest alcohol use (1–2 ounces a day):
raises HDL raises HDL
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Diet Diet
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Diet TherapyDiet Therapy 5–10% decrease in LDL cholesterol.5–10% decrease in LDL cholesterol. Should be assessed 4 weeks after initiation. Should be assessed 4 weeks after initiation. Reduce…Reduce…
Total daily fat to 25–30% Total daily fat to 25–30% Saturated fat to less than 7% of daily calories. Saturated fat to less than 7% of daily calories.
Dietary cholesterol less than 200 mg/d.Dietary cholesterol less than 200 mg/d. Polyunsaturated fats decrease LDL and Polyunsaturated fats decrease LDL and
HDLHDL Monounsaturated fats:Monounsaturated fats:
Decrease LDLDecrease LDL Increase HDL… GOOD!Increase HDL… GOOD!
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Diet TherapyDiet Therapy
"Mediterranean diet“, "Mediterranean diet“, monounsaturated fat such as that monounsaturated fat such as that found in canola oil and in olives, found in canola oil and in olives, peanuts, avocados, and their oils. peanuts, avocados, and their oils.
Soluble fiber, reduce LDL cholesterol Soluble fiber, reduce LDL cholesterol by 5–10%.by 5–10%.
Garlic, soy protein, vitamin C, pecans, Garlic, soy protein, vitamin C, pecans, and plant sterols.and plant sterols.
Antioxidants, found primarily in fruits Antioxidants, found primarily in fruits and vegetables. and vegetables.
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Pharmacologic Pharmacologic treatmenttreatment
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General measuresGeneral measures Aspirin prophylaxis at a dose of 81 mg/d.Aspirin prophylaxis at a dose of 81 mg/d. The therapeutic goal is:The therapeutic goal is:
Approached slowlyApproached slowly Watching for side effects.Watching for side effects. Encouraging adherence to nonpharmacologic Encouraging adherence to nonpharmacologic
Rx. Rx. Achieve a 30–40% reduction in LDL.Achieve a 30–40% reduction in LDL. Combinations of drugs may be necessary.Combinations of drugs may be necessary. Monitor periodically (every 6–8 weeks) Monitor periodically (every 6–8 weeks)
after starting therapy.after starting therapy.
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NIACIN (NICOTINIC NIACIN (NICOTINIC ACID)ACID)
Decrease the production of VLDL.Decrease the production of VLDL. Full-dose niacin therapy, 3–4.5 g/d Full-dose niacin therapy, 3–4.5 g/d 15–25% reduction in LDL cholesterol.15–25% reduction in LDL cholesterol. 25–35% increase in HDL cholesterol.25–35% increase in HDL cholesterol. Reduce triglycerides by half.Reduce triglycerides by half. Side effects:Side effects:
Flushing and pruritus. Less with aspirin 325 Flushing and pruritus. Less with aspirin 325 mg.mg.
Increase blood sugar.Increase blood sugar. Exacerbate gout and peptic ulcer disease.Exacerbate gout and peptic ulcer disease.
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BILE ACID-BINDING BILE ACID-BINDING RESINSRESINS
Cholestyramine and Colestipol.Cholestyramine and Colestipol. Decrease plasma LDL levels 15–25%.Decrease plasma LDL levels 15–25%. Increase Triglyceride level.Increase Triglyceride level. Don’t affects HDL.Don’t affects HDL. Side effects:Side effects:
constipation and gasconstipation and gas Nausea and vomiting.Nausea and vomiting. Absorption of fat-soluble vitamins.Absorption of fat-soluble vitamins.
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(HMG-COA) REDUCTASE (HMG-COA) REDUCTASE INHIBITORS (STATINS)INHIBITORS (STATINS)
atorvastatin, fluvastatin, lovastatin, atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin.pravastatin, rosuvastatin, and simvastatin.
Reduce MI and total mortality in secondary Reduce MI and total mortality in secondary prevention.prevention.
Significant reduction in risk of stroke.Significant reduction in risk of stroke. Decrease LDL level by up to 35%. Decrease LDL level by up to 35%. Increases HDL levels Increases HDL levels Decreases triglyceride levels. Decreases triglyceride levels. Myositis and hepatitis.Myositis and hepatitis. Monitor LFT’s Q 2-3 months then 2x/year if Monitor LFT’s Q 2-3 months then 2x/year if
stable.stable.
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Fibric Acid Derivatives Fibric Acid Derivatives
Gemfibrozil, Fenofibrate and Clofibrate.Gemfibrozil, Fenofibrate and Clofibrate. Increase the activity of LPL on VLDL.Increase the activity of LPL on VLDL. Reduce triglyceride levels by about 40%Reduce triglyceride levels by about 40% Reduce LDL levels by about 10–15%.Reduce LDL levels by about 10–15%. Raise HDL levels by about 15–20%. Raise HDL levels by about 15–20%. Side effects (mainly Clofibrate):Side effects (mainly Clofibrate):
cholelithiasis, hepatitis and hepatic cancer cholelithiasis, hepatitis and hepatic cancer and myositis.and myositis.
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EZETIMIBEEZETIMIBE
Inhibits the intestinal absorption of Inhibits the intestinal absorption of dietary and biliary cholesterol. dietary and biliary cholesterol.
Reduces LDL 15% - 20% when used Reduces LDL 15% - 20% when used as monotherapy.as monotherapy.
The usual dose of ezetimibe is 10 The usual dose of ezetimibe is 10 mg/d orally.mg/d orally.
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HDLHDL
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What increase What increase HDL?HDL?
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HDL increasesHDL increases
Nicotinic acidNicotinic acid Statins.Statins. Moderate alcohol intakeModerate alcohol intake GemfibrozilGemfibrozil ExerciseExercise Stopping smokingStopping smoking Losing weight. Losing weight.
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HDL decreases in …HDL decreases in …
Beta blockers (except Labetalol).Beta blockers (except Labetalol). SmokingSmoking High polyunsaturated diet.High polyunsaturated diet.
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High Blood Triglycerides High Blood Triglycerides
Risk for pancreatitis.Risk for pancreatitis. Treat fasting levels above 500 Treat fasting levels above 500
mg/dL.mg/dL.
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High Blood Triglycerides High Blood Triglycerides The primary therapy is dietary:The primary therapy is dietary:
Avoiding alcoholAvoiding alcohol Avoiding simple sugarsAvoiding simple sugars Avoiding refined starchesAvoiding refined starches Avoiding saturated trans fatty acids.Avoiding saturated trans fatty acids. Restricting total calories. Restricting total calories.
Medications: niacin, a fibric acid Medications: niacin, a fibric acid derivative, or an HMG-CoA reductase derivative, or an HMG-CoA reductase inhibitor.inhibitor.
Elevated TG increase CHD risk in men by Elevated TG increase CHD risk in men by 14% and in women by 37%.14% and in women by 37%.
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Metabolic syndromeMetabolic syndrome
25% of Americans25% of Americans 3 or more of the following:3 or more of the following:
1.1. Waist circumference > 102 cm in men or Waist circumference > 102 cm in men or > 88 cm in women> 88 cm in women
2.2. Serum triglyceride level of at least 150 Serum triglyceride level of at least 150 mg/dLmg/dL
3.3. HDL level of < 40 mg/dL in men or < 50 HDL level of < 40 mg/dL in men or < 50 mg/dL in women.mg/dL in women.
4.4. Blood pressure of at least 130/85 mm HgBlood pressure of at least 130/85 mm Hg5.5. Serum glucose level of at least 110 Serum glucose level of at least 110
mg/dL. mg/dL.
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NCEP ATP IIINCEP ATP III
1.1. TG (150–199 mg/dL): calorie TG (150–199 mg/dL): calorie restriction and exercise. restriction and exercise.
2.2. TG (> 200 mg/dL): Diet and TG (> 200 mg/dL): Diet and medications to make non-HDL medications to make non-HDL cholesterol 30 mg/dL higher than cholesterol 30 mg/dL higher than the LDL goal. the LDL goal.
Should be used for high risk Should be used for high risk patients. patients.
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ReferencesReferences CMDT 2007.CMDT 2007. Harrison’s principles of internal medicine.Harrison’s principles of internal medicine. MedStudy 2007/2008.MedStudy 2007/2008. Executive Summary of the Third Report of The Executive Summary of the Third Report of The
National Cholesterol Education Program (NCEP) National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol In Adults Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486–97.JAMA. 2001 May 16;285(19):2486–97. http://http://
www.nhlbi.nih.gov/guidelines/cholesterol/index.htmwww.nhlbi.nih.gov/guidelines/cholesterol/index.htm
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