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74 Cards in this Set
- Front
- Back
Goal 1
Know the goal levels for HDL, LDL, TG’s & TC |
Goals
LDL <130 (<100 optimal) HDL >40 TC <200 TG’s <150 |
|
Lipoproteins
LDL—”Bad cholesterol" |
-Primary target of antilipidemic drugs
-Makes up most of cholesterol in blood; -Increases risk of atherosclerotic CV disease |
|
What are the LDL Levels for
Optimal Above Optimal Borderline High High Very High |
<100 Optimal
100-129 Above optimal 130-159 Borderline high 160-189 High ≥190 Very high |
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Lipoproteins
HDL—”Good cholesterol” |
Increased levels = Potential decrease in coronary events
Decreased levels = Risk factor for coronary heart disease |
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What are the HDL levels for
Low High |
<40 Low
≥60 High |
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Triglycerides (TG’s)
|
Carried in blood by VLDL & IDL
Increased levels = Increased CV risk |
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TG's (mg/dL) Levels?
Normal Borderline high High Very high |
<150 Normal
150-199 Borderline high 200-499 High ≥500 Very high |
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Total Cholesterol (mg/dL)?
Optimal Borderline High |
<200 Optimal
200-239 Borderline high ≥ 240 High |
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Hypertriglyceridemia—Diagnosis
|
Screen for elevated cholesterol q5yrs in adults ≥20yrs of age
w/ Fasting Lipid profile (LDL, HDL, TC, TG’s) |
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Goal 2
Understand primary and secondary hyperlipidemia |
Primary -
Result of genetic defect in lipid metabolism or transport resulting in decreased LDL receptor activity, accumulation of LDL in blood and atherosclerosis Secondary- Diet (Most common cause) |
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Other causes of Secondary hyperlipidemia
|
Anorexia nervosa
Alcoholism - Hypertriglyceridemia Burns - Hypertriglyceridemia Cholestasis Chronic renal failure -Hypertriglyceridemia DM - Hypertriglyceridemia Growth hormone deficiency Hypoparathyroidism Pancreatitis Nephrotic syndrome Obstructive hepatic disease Medications (Steroids, corticosteroids, amiodarone, BB’s, cyclosporine, hormones, thiazides) |
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Increased levels apolipoprotein B?
|
primary protein of LDL, VLDL & IPL leads to an Increased risk of CHD
|
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Apolipoproteins
Increased levels apolipoprotein A? |
Associated w/increased levels of HDL & decreased risk of CHD
|
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Goal 3
Know the complications of hyperlipidemia |
and
how to calculate Framingham Risk score to assess 10yr risk |
|
CHD is complication of hyperlipidemia
Primary risk factors for CHD? |
Cigarette smoking
HTN BP ≥140/90 or on antihypertensive drug Low HDL (<40) Family hx premature CHD First-degree relative Male <55yrs old or female <65yrs Age males ≥45yrs old females ≥55yrs old |
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Negative risk factor for CHD?
|
HDL ≥60
|
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Additional risk factors for CHD
|
Obesity (BMI ≥30)
Lack of exercise Diet high in fat & TG’s High homocysteine levels Prothombotic issues Proinflammatory issues Impaired fasting glucose |
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5 Risk equivalents for CHD?
|
1.) Peripheral arterial disease
2.) Abdominal aortic aneurysm 3.) Carotid artery disease 4.) DM 5.) MI |
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Framingham Risk Calculation
counts which 6 major risk factors & to provide a 10yr risk assessment for CHD? |
age
gender TC smoking HDL SBP |
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Farmingham Risk goals
If 10yr risk >20% If 10yr risk 10-20% If 10yr risk <10% 0-1 Risk Factors |
If 10yr risk >20%, goal <70
If 10yr risk 10-20%, goal <100 If 10yr risk <10%: Goal <130 0-1 Risk Factors: Goal <160 |
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Goal 4
Know treatment goals for hyperlipidemia |
1.) Decrease s/sx, complications from hypertriglyceridemia
2.) Decrease risk of MI, UA, CVA, TIA from hyperlipidemia 3.) Reduce M&M from CHD 4.) Achieve goal LDL, HDL, TC & TG levels 5.) Choose most effective treatment with least amount of ADE’s and drug interactions for patient |
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Goal 5
Know the nonpharmacologic treatment for hyperlipidemia |
Hyperlipidemia—Pharmacologic Treatment
|
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LDL Goals for
if diagnosed with CDH or equivalent? |
Goal <100
|
|
Hyperlipidemia—Nonpharmacologic Treatment
Decrease dietary fat intake |
(≤25-35% total kcal)
<7% total daily calories from saturated fats ≤10% total daily calories from polyunsaturated fats ≤20% total daily calories from monounsaturated fats |
|
Hyperlipidemia—Nonpharmacologic Treatment
Carbohydrate intake & Protein intake |
CHO
50-60% total daily calories Protein 15% total daily calories |
|
Hyperlipidemia—Nonpharmacologic Treatment
Decrease dietary cholesterol intake |
(<200mg/dL)
|
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Hyperlipidemia—Nonpharmacologic Treatment
|
Increase fiber and plant sterols in diet to decrease LDL’s
Weight loss, maintain goal weight Exercise |
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Statins MOA?
|
Inhibits HMG Co-A reductase which is normally responsible for last step in cholesterol synthesis
Decrease LDL 18-55% Increase HDL 5-15% Decrease TG’s 7-30% |
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Statins ADE’s?
|
Pravastatin has least amount of ADE’s
GI upset (not very common) myalgias weakness rhabdomyolysis (serious, rare), increased LFT’s hepatotoxicity fatigue impotence |
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Statins Pharmacokinetics?
|
Absorption: Time to peak 1-2hrs
Metabolism: Hepatic except pravastatin (sulfation only) |
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Statins Drug Intxns?
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Gemfibrozil (increased risk of rhabdo),
azoles macrolides PI’s warfarin grapefruit juice |
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Statins Contraindications?
|
Hepatic dysfunction
pregnancy |
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Statins Monitoring?
|
LFT’s—Baseline, 6wks, 12wks
& 1-2 yrly D/C drug if LFT’s >3 times ULN |
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What is Rhabdomyolysis?
|
Rare serious condition
Risk inc. in ARF, myoglobinuria, hepatic dysfnxn, serious infxn, hypothyroidism, elderly S/sx: Muscle pain, weakness Monitoring: Check CPK level—If elevated, d/c drug |
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When should Statins be administered?
|
Administered once daily (all)
Should be administered at bedtime Most effective—cholesterol synthesis peaks at night Exception—atorvastatin (long-acting) |
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Name some Statins.
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Atorvastatin (Lipitor)
Fluvastatin (Lescol) Lovastatin (Mevacor) Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor) |
|
Fibrates/Fibric Acid Derivatives
MOA? |
Reduces hepatic lipogenesis rate
Can increase or decrease LDL Increase HDL 10-20% Decrease TG’s 20-50% |
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Fibrates ADE's?
|
GI upset (nausea, diarrhea, abdominal pain)
higher incidence of cholesectomy & appendectomy; gallstones myopathy; malignant GI disease (clofibrate) |
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Fibrate Drug interactions?
|
Statins (inc. risk of rhabdo)
warfarin (inc. INR) hypoglycemics (inc. hypoglycemia risk) |
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Fibrate Contraindications?
|
Severe renal dysfunction
severe hepatic dysfunction pregnancy gallbladder dz |
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Name some Fibrates?
|
Gemfibrozil (Lopid)
Fenofibrate (Tricor) |
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Niacin MOA?
|
Not considered 1st line treatment
Inhibits hepatic VLDL production |
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Niacin ADE’s
|
Flushing, pruritis
GI upset PUD exacerbation fatigue hyperglycemia hyperuricemia hepatotoxicity (inc. LFT’s) |
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Niacin Pharmacokinetics?
|
Absorption: Time to peak 30-60min
|
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Niacin Drug Intxns?
|
Statins (inc. risk of rhabdo)
|
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Niacin Contraindications?
|
PUD
gout hepatic dysfunction DM |
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How should Niacin be administered?
|
Take with food to avoid GI upset;
Take ASA 325mg po 30min prior to dose to avoid flushing & pruritis |
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Name some Niacin's?
|
Niacor (immediate release)
Niacin (immediate release, sustained release) Niaspan (extended release) |
|
Resins MOA?
|
Binds to bile acids to disrupt hepatic recirculation of bile acids; stimulates liver to convert hepatocellular cholesterol into bile acids
Decrease LDL 15-30% May increase HDL (3-5%) May increase TG’s |
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Resins ADE’s?
|
Nausea, constipation (20%), bloating, heartburn, bad taste
|
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Resins Drug Interactions?
|
Decreases absorption of other drugs—
warfarin, digoxin, thyroid, HCTZ, atbx, BB’s, statins, iron, Phb; Take dose 1hr prior to or 4hrs after other meds |
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Resins okay during pregnancy?
|
YES!!!
|
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Name some Resins
|
Cholestyramine
(Questran, Questran Light, Prevalite) Colestipol (Colestid) Colesevelam (Welchol) |
|
Ezetimibe (Zetia) MOA?
Adjunct statin therapy |
Inhibits cholesterol absorption from GI tract
Decrease LDL 15-20% May increase HDL 3% |
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Ezetimibe (Zetia) ADEs?
|
H/A, rash, diarrhea, myalgia
|
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Ezetimibe Drug Interactions?
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Gemfibrozil & clofibrate
(inc. risk of cholelithiasis) |
|
Fish Oil MOA?
|
Unknown; May reduce hepatic synthesis of TG’s
May decrease TG’s, lipoproteins Decrease VLDL Little effect on LDL May increase HDL |
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Fish Oil ADEs?
|
Thrombocytopenia,
impaired platelet fnxn, weight gain, impaired glucose tolerance, bad breath, oily stool, GI upset (burping, taste perversion, dyspepsia) |
|
Fish Oil Drug interactions?
|
None ID’d
Take with meals |
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Hyperlipidemia Clinical Course
|
1.) Check Framingham & 10-yr risk assessment for CHD
2.) Begin non-pharmacological treatment Diet 1st, then exercise & weight loss 3.) Initiate 1st line choice (statin, resin or niacin) 4.) If still not at goal after 6 wks, increase dose of statin if on or add resin or niacin; 5.) If still not at goal after 6 wks, add missing agent or further optimize dosages 6.) If still not at goal, refer to lipid specialist 7.)Monitor response q4-6mths |
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Which 1st line hyperlipidemic treatment significantly lowers LDL levels?
|
Statins
Atorvastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor) |
|
Which 1st line hyperlipidemic treatment
Demonstrate decreased major coronary events, CHD mortality, coronary procedures, stroke, total mortality? |
Statins
Atorvastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor) |
|
All statin's are have a hepatic metabolism except?
|
pravastatin (sulfation only)
|
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All statins should be administered at bedtime, except?
|
Exception—atorvastatin (long-acting)
|
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Classification of Hypertriglyceridemia?
|
Normal <150mg/dL
Borderline High 150-199mg/dL High 200-499mg/dL Very High ≥500mg/dL (watch for pancreatitis) |
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What are the contributing factors to Hypertriglyceridemia?
|
Obesity, inactivity, smoking, excess EtOH, DM, CRF, genetics
(familial hyperlipidemia), corticosteroids, hormones, BB’s) |
|
Treatment goals of severe hypertriglyceridemia?
|
Goal: To prevent acute pancreatitis
Restrict dietary fats to <15% of total daily calories Lower TG’s before LDL |
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What is the 1st line treatment for hypertriglyceridemia?
|
Niacin & fibrate
Niacin & fish oil for refractory patients |
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Which drug class should be AVOIDED in cases of hypertriglyceridemia?
|
Resins
Cholestyramine (Questran, Questran Light, Prevalite) Colestipol (Colestid) Colesevelam (Welchol) |
|
Which drug class used to treat Hyperlipidemia demonstrates a decrease in major coronary events, CHD mortality, and CAN be used during pregnancy?
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Resins
|
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What drug class is considered 1st line treatment for hypertriglyceridemia?
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Fibrates
Gemfibrozil (Lopid) Fenofibrate (Tricor) |
|
When is Niacin considered a best treatment option?
|
Ideal agent for patients with
low HDL & increased TG’s |
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At which dose does Niacin have to be given in order to see a cholestrol-lowering effect?
|
Cholesterol-lowering effect is dose-related; Not seen until dose at least 1500mg/day
|
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What is the first approved Omega-3 fatty acid approved for treatment of hypertriglyceridemia and hyperlipidemia?
|
Omega-3 Fatty Acids (Lovaza)
Decrease TG 45% Increase HDL 9% Increase LDL by as much as 45% |