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Pharmacology > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Definition and Etiologies of Hyperlipidemia

A 
Defined as serum cholesterol >200 mg/dL
Hyperlipidemia caused by:
Lifestyle choices
Poor diet choices
Lack of exercise
Secondary causes
Medications—antipsychotics (risperdone), prednisone, beta blockers (mildly), diuretics
Hypothyroidism
Genetics—familial hypercholesterolemia
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2
Q

**Emphasis: Untreated hyperlipids lead to….

A

Untreated hyperlipidemia causes atherosclerosis
Increases risk of:
MI
CVA

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3
Q

Hyperlipid Labs:

A

Testing includes:
Fasting total cholesterol, LDL, HDL, and triglycerides
Total cholesterol alone fine for screening, but does not give complete picutre

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4
Q

What is the focus of the new guidelines?

A

New guidelines available from American Heart Association/American College of Cardiology
Still somewhat controversial, do not focus on target LDL, rather looking at overall risk
More evidenced based than ATP III

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5
Q

Hyperlipid TX begins with…

A 
Starts with lifestyle changes
Dietary modifcations
Exercise program
Modifying alcohol intake
Evidence shows most patients still need a medication, even with adequate lifestyle changes
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6
Q

What is the goal for TX of hyperlipid?

A

Goal is to reduce relative risk of cardiac disease 20-30% regardless of their baseline LDL
Few studies show benefit of medications in those with a very low LDL (

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7
Q

Risk factors considering when treating hyperlipid:

A

Goal is to reduce relative risk of cardiac disease 20-30% regardless of their baseline LDL
Few studies show benefit of medications in those with a very low LDL (

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8
Q

What to use to assess risk:

A

Use the Framingham Scale to assess risk
Only good for patients 20 and older
Look at 10 year risk, not lifetime risk
Why? Few studies done on long term statin use. We know they have benefits very shortly after starting
Treat when risk of having a heart attack in the next 10 years is >20%

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9
Q

**Emphasis: At what % risk do you begin TX?

A

Treat when risk of having a heart attack in the next 10 years is >20%

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10
Q

If triglycerides are >500…

A

…treat triglycerides 1st

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11
Q

Determine goal of TX first-

A

Primary v. secondary
Primary: prevent a heart attack or stroke from happening in the first place
Secondary: prevent another heart attack or stroke

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12
Q

Specifics of Primary and Secondary TX goals:

A 
Primary: prevent a heart attack or stroke from happening in the first place
Typically a low to moderate dose statin
Pravastatin 20-40 mg
Atorvastatin 10 mg
Rosuvastatin 5-10 mg
Secondary: prevent another heart attack or stroke 
High dose statin
Pravastatin 40-80 mg
Atorvastatin 20-40 mg
Rosuvastatin 20-40 mg
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13
Q

**Emphasis: Post-MI pts ALWAYS need…

A

A HIGH DOSE STATIN ON TOP OF LIFESTYLE CHANGES!

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14
Q

List the 5 types of hyperlipidemia meds-

A
  1. HMG-CoA reductase inhibitors
  2. Ezetimibe (Zetia)
  3. Bile acid resins (Cholestyramine, Welchol)
  4. Niacin (nicotinic acid)
  5. Fibric acid derivatives (gemfibrozil, fenofibrate)
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15
Q

List the 5 types of hyperlipidemia meds-

A
  1. HMG-CoA reductase inhibitors (Statins)
  2. Ezetimibe (Zetia)
  3. Bile acid resins (Cholestyramine, Welchol)
  4. Niacin (nicotinic acid)
  5. Fibric acid derivatives (gemfibrozil, fenofibrate)
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16
Q

HMG-CoA reductase inhibitors- names, MOA, PK

A

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol)
GOLD STANDARD of high cholesterol treatment!
Mechanism of Action: competitive inhibitor of HMG-CoA, which produces cholesterol. By inhibiting this enzyme LDL production is decreased and more LDL is catabolized, decreasing LDL levels
ie, SOLELY TARGETS LDL
Pharmacokinetics:
Not well absorbed (14% bioavailability)
Metabolized in liver via CYP3A4 (except pravastatin)
Excreted in stool
Certain genotypes increase risk of toxicity, increased bioavailibility- ie, ASIANS/ELDERLY

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17
Q

GOLD STANDARD of high cholesterol treatment is:

A

STATINS!

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18
Q

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol): SE’s and C/I

A

Side effects: myopathy, arthralgias, diarrhea, increased LFTs
Monitoring parameters: LFTs, lipids, CPK
Contraindications: active liver disease, increased LFTs

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19
Q

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol): Monitoring parameters:

A

LFTs, lipids, CPK

20
Q

**Emphasis: Certain pts are at greater risk for toxicity from statins, who are they?

A

Certain genotypes increase risk of toxicity, increased bioavailibility- ie, ASIANS/ELDERLY

21
Q

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol): are the side effects related to dose?

A

the myopathies and arthralgias can be dose-dependent

22
Q

**Emphasis: what parameter are you especially wanting to follow, at initiation of RX and about 1 month?

A

LFT’s

23
Q

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol): Pregnancy, BFEED, PEDS

A

Not safe in pregnancy, breastfeeding, safe in pediatrics >10 years old (heterozygous familial hypercholesterolemia only)

24
Q

Simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol): best taken WHEN?

A

STATINS are best taken either with evening meal or at bedtime

25
Q

TO MIX OR NOT TO MIX?

Fibric acid derivatives and a statin?

A

NOT TO MIX!

26
Q

Starting a pt on a statin- dosing and education

A
  1. lowest dose
  2. QHS
  3. no grapefruit juice
  4. F/U in 1 month
  5. review SE’s ( esp. myopathies and arthralgias)
27
Q

If a pt cannot tolerate a statin, what is the next step?

A

Bile Acid Resins

28
Q

AZENTIDONONES: name, MOA, PK

A

Ezetimibe (Zetia)
Mechanism of Action: inhibits sterol transporter at brush border, which decreases intestinal absorption of cholesterol, thereby decreasing cholesterol deposition in liver and reduces cholesterol stores
Pharmacokinetics
Variable bioavailibility, food has no effect (cannot determine because insoluble in aqueous solution)
>90% protein bound
Metabolized primarily via glucuronide conjucation, also liver
Excreted primarily in stool

29
Q

Ezetimibe (Zetia): SE, C/I

A

Side effects: diarrhea, arthralgias, fatigue, increased LFTs (especially with reductase inhibitors)
Contraindications: active liver disease, unexplained increased LFTs

30
Q

**Emphasis: Monitoring parameters for Zetia?

A

Monitoring parameters: LFTs, lipids

31
Q

**Emphasis: what SE are you especially concerned about with Zetia?

A

Increasing LFTs!

32
Q

Ezetimibe (Zetia): SE, C/I

A

Side effects: diarrhea, arthralgias, fatigue, increased LFTs (especially with reductase inhibitors)
Contraindications: active liver disease, unexplained increased LFTs

33
Q

Ezetimibe (Zetia): Pregnancy, BFEED, PEDS

A

Category C in pregnancy, unknown if excreted in breastmilk (so avoid), safe in pediatrics >10 years old

34
Q

BILE ACID RESINS: Name, MOA, PK

A

Cholestyramine (Questran), colesevelam( WelChol)
Mechanism of Action: binds to bile salts to form an insoluble compound, inhibiting uptake of cholesterol
Pharmacokinetics
Minimally absorbed
Excreted in stool primarily, small amount in urine

35
Q

Cholestyramine (Questran), Colesevelam( WelChol): SE’s and C/I; monitoring parameters

A

Side Effects: constipation, GI upset
Monitoring Parameters: lipids
Contraindications: Coadministration with phenytoin, levothyroxine

36
Q

Cholestyramine (Questran), Colesevelam( WelChol): Pregnancy, BFEED, PEDS?

A

Safe in pregnancy, not excreted in breastmilk, safe in pediatrics >10 years old (heterozygous familial hypercholesterolemia only); cholestyramine safe in pediatrics

37
Q

**Emphasis: What is best choice in pregnancy for hyperlipidemia?

A

Cholestyramine (Questran), Colesevelam( WelChol)

38
Q

NICOTINIC ACID: Other name, MOA, PK

A 
Niacin, aka vitamin B3
Mechanism of Action: not well understood, but likely inhibits enzymes responsible for lipid synthesis
Pharmacokinetics
Good PO absorption
Unknown protein binding
Metabolized in liver
Excreted in urine
39
Q

Niacin/ Vit B3- SE’s, C/I, monitoring parameters

A

Side effects: flushing (decreased with extended-release preparations), increased LFTs, diarrhea, headache
Monitoring parameters: LFTs, lipids
Contraindications: liver disease

40
Q

**Emphasis: What two types of lipid meds are best for triglycerides?

A

Niacin or Fibric Acid

41
Q

Niacin/ Vit B3- Pregnancy, BFEED, PEDS

A

Safe in pregnancy at recommended doses (category A), Category C for doses >RDA, unknown if safe in breastfeeding, safe in pediatrics up to RDA (not a choice for cholesterol management however at the doses required)

42
Q

**Emphasis: What is the only lipid med that can increase HDL?

A

Fibric Acid derivatives (Tricor, Lopid)

43
Q

FIBRIC ACID DERIVATIVES: names, MOA, PK

A

Fenofibrate (Tricor), gemfibrozil (Lopid)
Mechanism of Action: inhibits peripheral lipolysis, as well as decreasing hepatic uptake of fatty acids. May also increase HDL via unknown mechanism
Pharmacokinetics
Close to 100% bioavailability
99% protein bound
Metabolized in liver
Excreted in urine

44
Q

Fenofibrate (Tricor), gemfibrozil (Lopid): SE’s, C/I

A

Side Effects: GI upset, increased LFTs, myalgias

Contraindications: severe liver disease, gallbladder disease

45
Q

**Emphasis: Fenofibrate (Tricor), gemfibrozil (Lopid): monitoring parameters

A

Monitoring Parameters: LFTs, CPK, lipids

46
Q

**Emphasis: Fenofibrate (Tricor), gemfibrozil (Lopid):

Pts to avoid use in

A

Always avoid using Tricor or Lopid in pts with hepatic or renal disease! Can increase kidney damage

47
Q

Fenofibrate (Tricor), gemfibrozil (Lopid): Pregnancy, BFEED, PEDS

A

Category C, unknown if excreted in breastmilk, not safe in pediatrics

Pharmacology (17 decks)

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