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Pharm Quiz 3 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Lipoproteins

A
  • Lipids (ex. cholesterol and triglycerides) are insoluble in plasma
  • Lipoproteins are responsible for carrying lipids to various tissues:

Energy utilization
Lipid deposition
Steroid hormone production
Bile acid formation

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2
Q

Hyperlipidemia

A

elevations in any lipoprotein species

a.k.a Hyperlipoproteinemia

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3
Q

Hyperlipemia

A

increased levels of triglycerides

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4
Q

Lipoprotein Structure

A
  1. Lipophilic core:
    Esterified cholesterol and Triglycerides
  2. Outer layer: Phospholipids and unesterfied cholesterol (hydrophilic)
  3. Apolipoproteins (apoproteins)
    Determines lipoprotein function
    –> Classification of lipoproteins
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5
Q

5 Classifications of Lipoproteins

A
  1. Chylomicrons
  2. Very low density lipoprotein (VLDL):
  3. Intermediate density lipoprotein (IDL)
  4. Low density lipoprotein (LDL)
  5. High density lipoprotein (HDL)
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6
Q

Chylomicrons

A

very large particles that carry dietary lipids

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7
Q

Very low density lipoprotein (VLDL):

A

carries triglycerides and to a lesser degree cholesterol

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8
Q

Intermediate density lipoprotein (IDL)

A

carries cholesterol esters and triglycerides

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9
Q

Low density lipoprotein (LDL)

A

carries cholesterol esters (Bad)

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10
Q

High density lipoprotein (HDL):

A

carries cholesterol esters

good

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11
Q

Apoprotein Function

A

Apoproteins B-100 and B48 convey lipids into the tissue and artery walls
- VLDL, IDL, LDL, chylomicrons

Plaque formation
–> Atherosclerosis

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12
Q

HDL Function:

A
  • Scavengers”
  • Acquire and transport cholesterol from atherosclerotic plaques and peripheral tissues to the liver
  • -> Reverse cholesterol transport
  • Elevated HDL reduces the risk of coronary heart disease (CHD)
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13
Q

Atherosclerosis

A
  • Leading cause of death in the US
  • Approximately 16.3% of U.S. adults have high cholesterol ≥ 240 mg/dL
    > 50% have a TC > 200 mg/dL
  • Estimated that < 50% of patients with elevated cholesterol are receiving pharmacotherapy
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14
Q

Who should receive a lipid panel?

A
  • Healthy adults over the age of 20 should receive a lipid panel every 5 years
  • Lipid panel should be obtained after a 9 to 12 hour fast
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15
Q

What is in a lipid panel?

A

Total cholesterol (TC)
Triglycerides
HDL
LDL and VLDL are calculated

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16
Q

How calculate VLDL?

A

VLDL = Triglycerides/5

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17
Q

How calculate LDL?

A

LDL=TC-(HDL+VLDL)

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18
Q

Primary hyperlipidemia

A

a.k.a. “familial” hyperlipidemia

Lipid metabolism defect
Fredrickson Classification (Type I-V)
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19
Q

Secondary hyperlipidemia

A

a.k.a. “acquired” hyperlipidemia

Diabetes
Hypothyroidism
Renal failure
Obstructive liver disease
Drugs induced (anabolic steroids, corticoid steroids, HIV protease inhibitors)
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20
Q

Step 1 for ATP III Cholesterol Guidelines

A

Determine lipoprotein levels:

LDL
< 100 Optimal
100-129: Near optimal/above optimal
130-159: Borderline High
160-189: high
>190: very high

HDL
< 40 Low
> 60 High

Total cholesterol: < 200 Desirable
200-239 Borderline high
> 240 High

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21
Q

Step 2 for ATP III Cholesterol Guidelines

A

Identify coronary heart disease (CHD) risk

Does the patient have any of the following?

  • Clinical CHD
  • Symptomatic carotid artery disease
  • Peripheral arterial disease
  • Abdominal aortic aneurysm
  • Diabetes
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22
Q

Step 3 for ATP III Cholesterol Guidelines

A

Determine presence of major risk factors:

  • Cigarette smoking
  • HTN or on antihypertensive meds
  • Low HDL
  • Family History of premature CHD (male < 55, femal < 65)
  • Age (men > 45, women > 55)
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23
Q

Step 4 for ATP III Cholesterol Guidelines

A

Assess 10-year CHD Risk –> Calculate Framingham Score if:
CHD or CHD risk equivalent
OR
2+ risk factors without CHD risk

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24
Q

Step 5 for ATP III Cholesterol Guidelines

A

Determine risk category

Risk category indicates:
LDL goal of therapy
Need for therapeutic lifestyle changes (TLC)
Level for drug consideration

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25
Q

Step 6 for ATP III Cholesterol Guidelines

A

Initiate TLC if LDL is above goal

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26
Q

Step 7 for ATP III Cholesterol Guidelines

A

Consider adding drug therapy

  • Consider drug simultaneously with TLC for CHD and CHD equivalents
  • Consider adding drug to after 3 months of TLC for other risk factors
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27
Q

Step 8 for ATP III Cholesterol Guidelines

A

Identify Metabolic Syndrome and treat

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28
Q

Step 9 for ATP III Cholesterol Guidelines

A

Treat elevated triglycerides

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29
Q

Framingham Risk Score

A 
Looks at to get 10 -year risk %:
Age
Total cholesterol
Smoking status
HDL
Systolic blood pressure

Low risk 20%

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30
Q

TLC Features

A

TLC Diet:

  • Saturated fat < 7%
  • Increased fiber

Weight management

Increased physical activity

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31
Q

Metabolic Syndrome

A
  • Abdominal Obesity (men: waist circumference > 102)
  • Triglycerides > 150
  • HDL < 40
  • BP > 130/85
  • Fasting Glucose > 110
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32
Q

Treating Metabolic Syndrome

A
  • Treat underlying causes (overweight, physical inactivity)
  • Treat lipic and non-lipid risk factors
    1. HTN
    2. Aspirin everyday for those with risk if CHD
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33
Q

Serum Triglycerides table

A

< 150 Norma
150-199 Borderline high
200-499 High
> 500 Very high

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34
Q

Non-HDL Goals

A

Non-HDL cholesterol=TC-HDL

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35
Q

Treating Elevated Triglycerides

A
  1. If triglycerides >500 mg/dL, first lower triglycerides to prevent pancreatitis:
    - Very low-fat diet (<500 mg/dL, turn to LDL-lowering therapy
  2. If triglycerides 200-499 mg/dL after LDL goal is reached, consider adding drug if needed to reach non-HDL goal
    - Intensify therapy with LDL-lowering drug, or
    - Add nicotinic acid or fibrate to further lower VLDL
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36
Q

Therapeutic Lifestyle Changes

A

Initial treatment of choice:

Weight management
Physical activity
TLC diet
Smoking cessation
Managing other comorbidities (hypertension, diabetes)
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37
Q

Pharmacologic Therapy

A 
HMG-CoA reductase inhibitors
Niacin (nicotinic acid)
Fibric acid derivatives (Fibrates)
Bile acid-binding resins
Inhibitors of intestinal sterol absorption
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38
Q

HMG-CoA reductase inhibitors effect

A

↓LDL 20-50%
↑ HDL 10%
↓ TG’s 10-20%

39
Q

HMG-CoA reductase inhibitors MOA

A

Reduce hepatic cholesterol biosynthesis
Analogs of an HMG-CoA intermediate
“Statins”

40
Q

Detailed HMG-CoA reductase inhibitors MOA

A
  1. Increase in high-affinity LDL receptors –>
  2. Increases the fractional catabolic rate of LDL
    and Increases the liver’s extraction of LDL precursors –>
  3. Reduce LDL
41
Q

Other beneficial effects of statins:

A

Decrease oxidative stress
Decrease vascular inflammation
Stabilize of atherosclerotic lesions

42
Q

Pharmacokinetics of statins

A
  • Bioavailability varies from 40% to 75%
    Exception: fluvastatin ~100% absorbed
  • High first-pass extraction by the liver
    Hepatic CYP3A4
  • Half-lives range from 1 to 3 hours
    Exceptions: atorvastatin (14 hrs), pitavastatin (12 hrs), and rosuvastatin (19 hrs)
43
Q

Administration of statins

A
  • Once daily
  • Most effective if taken in the evening
    Endogenous cholesterol production occurs at night
  • Grapefruit juice? –> inhibits enzyme that breaks down statins so statin levels rise
44
Q

Adverse Effects of statins

A
  • Hepatic dysfunction- elevated liver function tests (LFTs)
    Aminotransferase most commonly
  • Discontinue therapy if levels are elevated >3 times the upper limit or normal
  • Contraindication: active or chronic liver disease
  • Myopathy- increase creatinine kinase (CK)
    Dose-related
    At risk: age ≥65, females, uncontrolled hypothyroidism, and renal dysfunction
  • Discontinue use if symptomatic and CK activity is elevated
    Rechallenge with same or alternative statin
45
Q

Monitoring of statins

A
  • Lipid panel 6-8 weeks after initiation of drug therapy or dosage change
    Every 6 months to annually thereafter
  • Obtain baseline CK and liver function test
    Recheck only if patient is symptomatic or if clinically indicated
46
Q

Drug interactions of statins

A
  • CYP3A4 Inhibitors (statins rise):
    Macrolide antibiotics, cyclosporine, ketoconazole,tacrolimus,nefazodone, fibrates,paroxetine,venlafaxine
  • CYP3A4 Inducers (statins decrease):
    Phenytoin, griseofulvin, barbiturates, rifampin, and thiazolidinediones
47
Q

Atorvastatin(Lipitor®)

A

10, 20, 40, 80 mg tablets

48
Q

Lovastatin*(Mevacor®)

A

10, 20, 40 mg tablets

49
Q

Rosuvastatin(Crestor®)

A

5, 10, 20, 40 mg tablets

50
Q

Niacin (nicotinic acid) effects

A

↓ LDL 10-15%
↑ HDL 10%
↓ TG’s 20-80%

51
Q

Niacin (nicotinic acid) MOA

A

Reduces hepatic VLDL secretion & enhances VLDL clearance

Therefore reducing LDL

52
Q

Niacin (nicotinic acid) Pharmacokinetics

A
  • Time to peak
    IR formulation: 30-60 minutes
    ER formulation: 4-5 hours
  • Extensive first-pass effects: Converted to the amide form
    Nicotinamide adenine dinucleotide (NAD), nicotinuric acid, and other metabolites
    – Excreted in the urine
53
Q

Niacin (nicotinic acid) IR formulation Administration

A

Initial: 200-300mg/day in divided doses
Increase dose every 4-7 days to response
Therapeutic dose: 1.5-3 g/day in 2-3 divided doses (max dose: 4.5g/day)

54
Q

Niacin (nicotinic acid) ER formulation Administration

A

Initial: 500 mg once daily at bedtime
Increase every 4 weeks until therapeutic
Maximum of 2 g/day

55
Q

Niacin (nicotinic acid) ADR

A 
Flushing, pruruitus, warmth, tingling
Hyperglycemia
Hyperuricemia (or gout)
Upper GI distress
Hepatotoxicity
56
Q

Niacin (nicotinic acid) Monitoring

A
  • Obtain liver function tests at baseline
    Recheck every 6-12 weeks for first year, then periodically (approximately every 6 months)
  • Uric acid if symptomatic of gout
  • Blood glucose in diabetic patients
57
Q

Niacin (nicotinic acid) Drug Interactions

A
  • Bile acid-binding resins
    May decrease the absorption of Niacin
  • HMG-CoA Reductase Inhibitors
    Niacin may enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors
58
Q

Niacin (nicotinic acid) Immediate Release (OTC)

A

Niacin (Vitamin B3)

50 mg, 100 mg, 250 mg, 500 mg

59
Q

Niacin (nicotinic acid) Extended Release

A

Niacor®, Niaspan® (RX)
500 mg, 750 mg, 1000 mg

Slo-Niacin (OTC)
500 mg, 750 mg

60
Q

How to lessen ADR of Niacin (nicotinic acid)?

A
  • Pretreat with aspirin (1 hr before)
  • Try ER type
  • Take before bed
  • Avoid EtOH, hot showers, spicy foods
61
Q

Fibric acid derivatives (Fibrates) Effects

A

↓ LDL 10%
↑ HDL 10-25%
↓ TG’s 40-50%

62
Q

Fibric acid derivatives (Fibrates) MOA

A

Activate lipoprotein lipase
Promote delivery of TG’s to adipose
Interfere with VLDL formation in the liver

63
Q

Fibric acid derivatives (Fibrates) Pharmacokinetics

A
  • Absorption is increased with meals
  • Tightly bound to plasma proteins
  • Undergoes enterohepatic circulation
  • Half-life is 20 hours
  • Excreted in the urine (60-70%) as the glucuronide, and about 25% in feces
64
Q

Fibric acid derivatives (Fibrates) Drugs

A
  • Fenofibrate
  • Gemfibrizol
  • Lopid®
65
Q

Fibric acid derivatives (Fibrates) Administration Fenofibrate

A
  • Orally, once daily with food
  • MANY preparations and strengths
  • Adjusted for renal function:
    Clcr>80 mL/minute: No dosage adjustment
    Clcr31-80 mL/minute: Adjust dose
    Clcr≤30 mL/minute: Use is contraindicated
66
Q

Fibric acid derivatives (Fibrates) Administration Gemifibrizol

A

600 mg twice daily

Administer 30 minutes before breakfast and dinner

67
Q

Fibric acid derivatives (Fibrates) Preparations

A

Lopid®: 600 mg

Available as generic

68
Q

Fibric acid derivatives (Fibrates) ADR

A 
Rare:
Gastrointestinal symptoms
Myopathy
Arrhythmias
Elevated aminotransferases or alkaline phosphatase
69
Q

Fibric acid derivatives (Fibrates) Monitoring

A

Lipid panel at baseline, 3 and 6 months
LFTs periodically
Serum creatinine (SCr)

70
Q

Fibric acid derivatives (Fibrates) Drug interactions

A
  • Statins –> myopathies
    Fibrate is preferred over gemfibrizol
  • Bile acid-binding resins
    Separate doses by 2 hrs
  • Warfarin: ↑ warfarin effect
71
Q

Bile acid-binding resins MOA

A 
Non-absorbable anion exchange resins
Inhibits enterohepatic recycling
Bile excretion ↑ and ↓ cholesterol pool in liver
LDL receptors upregulate
LDL clearance increases
72
Q

Bile acid-binding resins Effect

A

↓ LDL 10-20%
↑ HDL 0-2%
↑ TG’s 0-5%

73
Q

Bile acid-binding resins Pharmacokinetics

A

Resin is not absorbed systemically
Remains in the gut
Eliminated in feces

74
Q

Bile acid-binding resins Administration

A
  • Decrease absorption of other medications
    Do not take any other medication 1 hour before or 2 hours after
  • Tablets: Administer with a meal
    LARGE tablet –> if trouble swallowing, recommend suspension form
75
Q

Bile acid-binding resins ADR

A

GI discomfort:

  • Bloating
  • Nausea
  • -Heartburn
  • Constipation

Hypertriglyceridemia
- Contraindicated in hyperlipemia (>400mg/dL)

76
Q

Bile acid-binding resins Monitoring

A
  • Effect on LDL in ~2 weeks
  • Lipid panel at baseline
    Every 6 months to 1 year after therapeutic
77
Q

Bile acid-binding resins Drug Interactions

A 
Digoxin
Thiazides
Warfarin
Thyroxine
Aspirin
Pravastatin
Fluvastatin
Ezetimibe
Iron salts
Fat soluble viatmins
78
Q

Bile acid-binding resins Preparations

A

Cholestyramine (Questran®)
4g packet or bulk powder

Colestipol (Colestid®)
1gm tablet, 5g powder packet

Colesevelam (WelChol®)
625mg tablet, 3.75g powder packet

79
Q

Inhibitors of intestinal sterol absorption MOA

A

Selective inhibition of intestinal absorption of dietary cholesterol

Effective even in the absence of dietary cholesterol  inhibits reabsorption of cholesterol excreted in the bile

80
Q

Inhibitors of intestinal sterol absorption Effects

A

↓ LDL 17%
↑ HDL 1.3%
↓ TG’s 6%

81
Q

Inhibitors of intestinal sterol absorption Pharmacokinetics

A
  • Readily absorbed
  • Conjugated in the intestine to an active glucuronide
  • Undergoes enterohepatic circulation
  • Half-life=22 hours, peak in 4-12 hours
  • Excreted in feces (78%)
82
Q

Inhibitors of intestinal sterol absorption Administration

A

Single daily dose of 10 mg without regard to meals

83
Q

Inhibitors of intestinal sterol absorption ADR

A 
Diarrhea
Abdominal pain
Arthralgia
Back pain
Fatigue
84
Q

Inhibitors of intestinal sterol absorption Monitoring

A
  • Lipid panel at baseline, 6 weeks after initiation, then every 6 months to annually
    When in combination with fenofibrate
  • Monitor LFTs and signs and symptoms of cholelithiasis
85
Q

Inhibitors of intestinal sterol absorption Drug interactions

A 
- Fibrates
Cholelithiasis, myopathy
- Bile acid-binding resins
- Lovastatin ER, Niacin
Myopathy
86
Q

Inhibitors of intestinal sterol absorption Preparations

A

Currently only one available

Ezetimibe (Zetia®) 10mg tablet

87
Q

Fish Oil (omega 3 fatty acids)

A
  • May decrease triglycerides
  • Unpleasant side effect profile:
    Belching, flatulence, indigestion, altered taste
88
Q

Fish Oil (omega 3 fatty acids) Contraindicated

A

Fish allergy

Coagulopathies

89
Q

Fish Oil (omega 3 fatty acids) Preparations

A

Lovaza® 4g daily (or 2g twice daily)

90
Q

Pregnancy/lactation options

A
  • Statins are contraindicated (category X)

Options:

  • Colesevelam (category B)
  • Fenofibrate, gemfibrozil, niacin, cholestyramine, ezetimibe (category C)
91
Q

Children options

A

Diet and lifestyle modifications first line

Drug of choice: cholestyramine

92
Q

Best for LDL

A

Statins: largest reduction in LDL

93
Q

Best for Triglycerides

A

Niacin, fibrates

NOT bile acid-binding resins

94
Q

What if not at goal?

A

Statin + bile acid-binding resin
Statin + ezetimibe
Statin + niacin
Statin + fibrate (not gemfibrizol)

Pharm Quiz 3 (4 decks)

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