Hyperlipidemia Slides 1-27

Front 1

Goal 1

Know the goal levels for HDL, LDL, TG’s & TC

Back 1

Goals
LDL <130 (<100 optimal)
HDL >40
TC <200
TG’s <150

Front 2

Lipoproteins

LDL—”Bad cholesterol"

Back 2

-Primary target of antilipidemic drugs
-Makes up most of cholesterol in blood; -Increases risk of atherosclerotic CV disease

Front 3

What are the LDL Levels for

Optimal
Above Optimal
Borderline High
High
Very High

Back 3

<100 Optimal
100-129 Above optimal
130-159 Borderline high
160-189 High
≥190 Very high

Front 4

Lipoproteins

HDL—”Good cholesterol”

Back 4

Increased levels = Potential decrease in coronary events

Decreased levels = Risk factor for coronary heart disease

Front 5

What are the HDL levels for

Low
High

Back 5

<40 Low
≥60 High

Front 6

Triglycerides (TG’s)

Back 6

Carried in blood by VLDL & IDL

Increased levels = Increased CV risk

Front 7

TG's (mg/dL) Levels?
Normal
Borderline high
High
Very high

Back 7

<150 Normal
150-199 Borderline high
200-499 High
≥500 Very high

Front 8

Total Cholesterol (mg/dL)?

Optimal
Borderline
High

Back 8

<200 Optimal
200-239 Borderline high
≥ 240 High

Front 9

Hypertriglyceridemia—Diagnosis

Back 9

Screen for elevated cholesterol q5yrs in adults ≥20yrs of age
w/
Fasting Lipid profile (LDL, HDL, TC, TG’s)

Front 10

Goal 2

Understand primary and secondary hyperlipidemia

Back 10

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)

Front 11

Other causes of Secondary hyperlipidemia

Back 11

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)

Front 12

Increased levels apolipoprotein B?

Back 12

primary protein of LDL, VLDL & IPL leads to an Increased risk of CHD

Front 13

Apolipoproteins

Increased levels apolipoprotein A?

Back 13

Associated w/increased levels of HDL & decreased risk of CHD

Front 14

Goal 3

Know the complications of hyperlipidemia

Back 14

and
how to calculate Framingham Risk score to assess 10yr risk

Front 15

CHD is complication of hyperlipidemia

Primary risk factors for CHD?

Back 15

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

Front 16

Negative risk factor for CHD?

Back 16

HDL ≥60

Front 17

Additional risk factors for CHD

Back 17

Obesity (BMI ≥30)
Lack of exercise
Diet high in fat & TG’s
High homocysteine levels
Prothombotic issues
Proinflammatory issues
Impaired fasting glucose

Front 18

5 Risk equivalents for CHD?

Back 18

1.) Peripheral arterial disease
2.) Abdominal aortic aneurysm
3.) Carotid artery disease
4.) DM
5.) MI

Front 19

Framingham Risk Calculation

counts which 6 major risk factors & to provide a 10yr risk assessment for CHD?

Back 19

age
gender
TC
smoking
HDL
SBP

Front 20

Farmingham Risk goals

If 10yr risk >20%
If 10yr risk 10-20%
If 10yr risk <10%

0-1 Risk Factors

Back 20

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

Front 21

Goal 4

Know treatment goals for hyperlipidemia

Back 21

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

Front 22

Goal 5

Know the nonpharmacologic treatment for hyperlipidemia

Back 22

Hyperlipidemia—Pharmacologic Treatment

Front 23

LDL Goals for

if diagnosed with CDH or equivalent?

Back 23

Goal <100

Front 24

Hyperlipidemia—Nonpharmacologic Treatment

Decrease dietary fat intake

Back 24

(≤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

Front 25

Hyperlipidemia—Nonpharmacologic Treatment

Carbohydrate intake &
Protein intake

Back 25

CHO
50-60% total daily calories
Protein
15% total daily calories

Front 26

Hyperlipidemia—Nonpharmacologic Treatment

Decrease dietary cholesterol intake

Back 26

(<200mg/dL)

Front 27

Hyperlipidemia—Nonpharmacologic Treatment

Back 27

Increase fiber and plant sterols in diet to decrease LDL’s

Weight loss, maintain goal weight

Exercise

Front 28

Statins MOA?

Back 28

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%

Front 29

Statins ADE’s?

Back 29

Pravastatin has least amount of ADE’s

GI upset (not very common)
myalgias
weakness
rhabdomyolysis (serious, rare), increased LFT’s
hepatotoxicity
fatigue
impotence

Front 30

Statins Pharmacokinetics?

Back 30

Absorption: Time to peak 1-2hrs

Metabolism: Hepatic
except pravastatin (sulfation only)

Front 31

Statins Drug Intxns?

Back 31

Gemfibrozil (increased risk of rhabdo),
azoles
macrolides
PI’s
warfarin
grapefruit juice

Front 32

Statins Contraindications?

Back 32

Hepatic dysfunction

pregnancy

Front 33

Statins Monitoring?

Back 33

LFT’s—Baseline, 6wks, 12wks
& 1-2 yrly

D/C drug if LFT’s >3 times ULN

Front 34

What is Rhabdomyolysis?

Back 34

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

Front 35

When should Statins be administered?

Back 35

Administered once daily (all)

Should be administered at bedtime

Most effective—cholesterol synthesis peaks at night

Exception—atorvastatin (long-acting)

Front 36

Name some Statins.

Back 36

Atorvastatin (Lipitor)
Fluvastatin (Lescol)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Rosuvastatin (Crestor)
Simvastatin (Zocor)

Front 37

Fibrates/Fibric Acid Derivatives

MOA?

Back 37

Reduces hepatic lipogenesis rate

Can increase or decrease LDL
Increase HDL 10-20%
Decrease TG’s 20-50%

Front 38

Fibrates ADE's?

Back 38

GI upset (nausea, diarrhea, abdominal pain)

higher incidence of cholesectomy & appendectomy;

gallstones
myopathy;
malignant GI disease (clofibrate)

Front 39

Fibrate Drug interactions?

Back 39

Statins (inc. risk of rhabdo)

warfarin (inc. INR)

hypoglycemics (inc. hypoglycemia risk)

Front 40

Fibrate Contraindications?

Back 40

Severe renal dysfunction
severe hepatic dysfunction
pregnancy
gallbladder dz

Front 41

Name some Fibrates?

Back 41

Gemfibrozil (Lopid)
Fenofibrate (Tricor)

Front 42

Niacin MOA?

Back 42

Not considered 1st line treatment

Inhibits hepatic VLDL production

Front 43

Niacin ADE’s

Back 43

Flushing, pruritis
GI upset
PUD exacerbation
fatigue
hyperglycemia
hyperuricemia
hepatotoxicity (inc. LFT’s)

Front 44

Niacin Pharmacokinetics?

Back 44

Absorption: Time to peak 30-60min

Front 45

Niacin Drug Intxns?

Back 45

Statins (inc. risk of rhabdo)

Front 46

Niacin Contraindications?

Back 46

PUD
gout
hepatic dysfunction
DM

Front 47

How should Niacin be administered?

Back 47

Take with food to avoid GI upset;

Take ASA 325mg po 30min prior to dose to avoid flushing & pruritis

Front 48

Name some Niacin's?

Back 48

Niacor (immediate release)

Niacin (immediate release, sustained release)

Niaspan (extended release)

Front 49

Resins MOA?

Back 49

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

Front 50

Resins ADE’s?

Back 50

Nausea, constipation (20%), bloating, heartburn, bad taste

Front 51

Resins Drug Interactions?

Back 51

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

Front 52

Resins okay during pregnancy?

Back 52

YES!!!

Front 53

Name some Resins

Back 53

Cholestyramine
(Questran, Questran Light, Prevalite)

Colestipol (Colestid)
Colesevelam (Welchol)

Front 54

Ezetimibe (Zetia) MOA?

Adjunct statin therapy

Back 54

Inhibits cholesterol absorption from GI tract

Decrease LDL 15-20%
May increase HDL 3%

Front 55

Ezetimibe (Zetia) ADEs?

Back 55

H/A, rash, diarrhea, myalgia

Front 56

Ezetimibe Drug Interactions?

Back 56

Gemfibrozil & clofibrate

(inc. risk of cholelithiasis)

Front 57

Fish Oil MOA?

Back 57

Unknown; May reduce hepatic synthesis of TG’s

May decrease TG’s, lipoproteins
Decrease VLDL
Little effect on LDL
May increase HDL

Front 58

Fish Oil ADEs?

Back 58

Thrombocytopenia,
impaired platelet fnxn,
weight gain,
impaired glucose tolerance,
bad breath,
oily stool, GI upset

(burping, taste perversion, dyspepsia)

Front 59

Fish Oil Drug interactions?

Back 59

None ID’d

Take with meals

Front 60

Hyperlipidemia Clinical Course

Back 60

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

Front 61

Which 1st line hyperlipidemic treatment significantly lowers LDL levels?

Back 61

Statins

Atorvastatin (Lipitor)
Fluvastatin (Lescol)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Rosuvastatin (Crestor)
Simvastatin (Zocor)

Front 62

Which 1st line hyperlipidemic treatment

Demonstrate decreased major coronary events, CHD mortality, coronary procedures, stroke, total mortality?

Back 62

Statins

Atorvastatin (Lipitor)
Fluvastatin (Lescol)
Lovastatin (Mevacor)
Pravastatin (Pravachol)
Rosuvastatin (Crestor)
Simvastatin (Zocor)

Front 63

All statin's are have a hepatic metabolism except?

Back 63

pravastatin (sulfation only)

Front 64

All statins should be administered at bedtime, except?

Back 64

Exception—atorvastatin (long-acting)

Front 65

Classification of Hypertriglyceridemia?

Back 65

Normal <150mg/dL

Borderline High 150-199mg/dL

High 200-499mg/dL

Very High ≥500mg/dL
(watch for pancreatitis)

Front 66

What are the contributing factors to Hypertriglyceridemia?

Back 66

Obesity, inactivity, smoking, excess EtOH, DM, CRF, genetics

(familial hyperlipidemia), corticosteroids, hormones, BB’s)

Front 67

Treatment goals of severe hypertriglyceridemia?

Back 67

Goal: To prevent acute pancreatitis

Restrict dietary fats to <15% of total daily calories

Lower TG’s before LDL

Front 68

What is the 1st line treatment for hypertriglyceridemia?

Back 68

Niacin & fibrate

Niacin & fish oil for refractory patients

Front 69

Which drug class should be AVOIDED in cases of hypertriglyceridemia?

Back 69

Resins

Cholestyramine (Questran, Questran Light, Prevalite)
Colestipol (Colestid)
Colesevelam (Welchol)

Front 70

Which drug class used to treat Hyperlipidemia demonstrates a decrease in major coronary events, CHD mortality, and CAN be used during pregnancy?

Back 70

Resins

Front 71

What drug class is considered 1st line treatment for hypertriglyceridemia?

Back 71

Fibrates
Gemfibrozil (Lopid)
Fenofibrate (Tricor)

Front 72

When is Niacin considered a best treatment option?

Back 72

Ideal agent for patients with
low HDL
&
increased TG’s

Front 73

At which dose does Niacin have to be given in order to see a cholestrol-lowering effect?

Back 73

Cholesterol-lowering effect is dose-related; Not seen until dose at least 1500mg/day

Front 74

What is the first approved Omega-3 fatty acid approved for treatment of hypertriglyceridemia and hyperlipidemia?

Back 74

Omega-3 Fatty Acids (Lovaza)

Decrease TG 45%
Increase HDL 9%
Increase LDL by as much as 45%