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Pharmacotherapy II > Hyperlipidemia Weber Exam 3 > Flashcards

Hyperlipidemia Weber Exam 3 Flashcards

1
Q

What gender has an earlier occurrence of HLD? What gender has a higher prevalence of HLD?

A

Men earlier occurrence; women higher prevalence.

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2
Q

What gender has an earlier occurrence of HLD? What gender has a higher prevalence of HLD?

A

Men earlier occurrence; women higher prevalence.

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3
Q

What is the pathogenic process for atherosclerosis development?

A

Endothelial injury (LDL infiltrates), then inflammatory response, macrophages infiltrate, platelet adhesion, smooth muscle cell proliferation, extracellular matrix accumulation.

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4
Q

What impact does malnutrition have on LDL and HDL?

A

Decreases both of them

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5
Q

What thyroid condition can elevate LDL?

A

Hypothyroidism

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6
Q

What are potential drug causes of elevated LDL?

A

Thiazides, cyclosporine, tegretol

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7
Q

What are some (more uncommon) signs of hyperlipidemia?

A

Pancreatitis, xanthomas, peripheral polyneuropathy, increased BP, waist size >40 inches in men, >35 inches in women, BMI >30kg/m2

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8
Q

What is one easy physical assessment technique to look for the presence of vascular disease?

A

Ankle-brachial index–involves taking BP in arm and ankle, the ratio should be >0.9-1.3 in healthy people, lower in vascular disease.

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9
Q

What is an LDL-P?

A

The number of LDL particles (can tell you particle size)

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10
Q

How is non-HDL-C calculated? What does it represent?

A

Non-HDL-C = TC - HDL. Represents amount of cholesterol in atherogenic particles.

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11
Q

What lipid panel measurements are valid in non-fasting state?

A

TC, HDL, LDL-P, ApoB

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12
Q

How is LDL-C estimated in a lipid panel?

A

Friedewald equation:

LDL = TC - HDL - TG/5

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13
Q

When is the Friedewald equation not valid?

A

When TG > 400mg/dL

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14
Q

What additional factors does the pooled cohort equation consider in addition to gender, age, TC, HDL, SBP, smoking status, and treatment for HTN?

A

Race and DM

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15
Q

What is a goal TC/HDL?

A
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16
Q

What additional factors does the pooled cohort equation consider in addition to gender, age, TC, HDL, SBP, smoking status, and treatment for HTN?

A

Race and DM

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17
Q

What is the pathogenic process for atherosclerosis development?

A

Endothelial injury (LDL infiltrates), then inflammatory response, macrophages infiltrate, platelet adhesion, smooth muscle cell proliferation, extracellular matrix accumulation.

How well did you know this?
1
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2
3
4
5
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18
Q

What impact does malnutrition have on LDL and HDL?

A

Decreases both of them

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19
Q

What thyroid condition can elevate LDL?

A

Hypothyroidism

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20
Q

What are potential drug causes of elevated LDL?

A

Thiazides, cyclosporine, tegretol

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21
Q

What are some (more uncommon) signs of hyperlipidemia?

A

Pancreatitis, xanthomas, peripheral polyneuropathy, increased BP, waist size >40 inches in men, >35 inches in women, BMI >30kg/m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is one easy physical assessment technique to look for the presence of vascular disease?

A

Ankle-brachial index–involves taking BP in arm and ankle, the ratio should be >0.9-1.3 in healthy people, lower in vascular disease.

How well did you know this?
1
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2
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4
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23
Q

In a diabetic patient with elevated triglycerides, what might be the root cause?

A

Uncontrolled blood glucose can elevate triglycerides.

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24
Q

A patient taking simvastatin (Zocor) 40mg begins to experience myalgia. The doctor wants to switch to a less lipophilic patient. Which would be an equivalent dose?

a) Rosuvastatin (Crestor) 10mg
b) Pitavastatin (Livalo) 4mg
c) Pravastatin (Pravachol) 40mg
c) Atorvastatin (Lipitor) 40mg

A

b) Pitavastatin 4mg

* atorvastatin would have the same problem!*

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25
Q

During a follow up visit with a patient, you discover that the fluvastatin (Lescol) 80mg that you prescribed is not working because the patient is not able to take it at night. What is an equivalent dose?

a) Rosuvastatin (Crestor) 5mg
b) Lovastatin (Altoprev/Mevacor) 80mg
c) Pravastatin (Pravachol) 20mg
d) Atorvastatin (Lipitor) 10mg

A

d) Atorvastatin 10mg

* lovastatin would have the same problem!*

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26
Q

True or false: Pitavastatin and pravastatin absorption is enhanced by food, but lovastatin absorption is decreased by food.

A

False–lovastatin needs to be taken with evening meal to increase absorption, but pitavastatin and pravastatin should not be taken near a meal.

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27
Q

When is the Friedewald equation not valid?

A

When TG > 400mg/dL

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28
Q

What clinical trial first discovered an increase in blood sugars and DM with rosuvastatin therapy?

A

JUPITER

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29
Q

What additional factors does the pooled cohort equation consider in addition to gender, age, TC, HDL, SBP, smoking status, and treatment for HTN?

A

Race and DM

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30
Q

What is a goal TC/HDL?

A
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31
Q

When recommending non-PCOL changes, how should your recommendations always be made?

A

Always be specific and always tailor to the patient

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32
Q

What diets have potential for HLD?

A

DASH, USDA food pattern, or AHA diet (all increase veggies, fruits, whole grains, dairy, nuts, and limit sweets/red meats)

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33
Q

What is a good sodium intake goal?

A
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34
Q

What patient population should NEVER receive statins?

A

Pregnant women

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35
Q

Name some soluble fibers that can decrease LDL.

A

Oat bran, pectins/gums, psyllium products

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36
Q

What meat should be eaten at least once weekly to reduce CV mortality?

A

Fish

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37
Q

What OTC supplement might be a culprit in increasing LDL?

A

Fish oil/omega 3 fatty acids

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38
Q

In a diabetic patient with elevated triglycerides, what might be the root cause?

A

Uncontrolled blood glucose can elevate triglycerides.

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39
Q

A patient taking simvastatin 40mg begins to experience myalgia. The doctor wants to switch to a less lipophilic patient. Which would be an equivalent dose?

a) Rosuvastatin 10mg
b) Pitavastatin 4mg
c) Pravastatin 40mg
c) Atorvastatin 40mg

A

b) Pitavastatin 4mg

* atorvastatin would have the same problem!*

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40
Q

During a follow up visit with a patient, you discover that the fluvastatin 80mg that you prescribed is not working because the patient is not able to take it at night. What is an equivalent dose?

a) Rosuvastatin 5mg
b) Lovastatin 80mg
c) Pravastatin 20mg
d) Atorvastatin 10mg

A

d) Atorvastatin 10mg

* lovastatin would have the same problem!*

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41
Q

True or false: Pitavastatin and pravastatin absorption is enhanced by food, but lovastatin absorption is decreased by food.

A

False–lovastatin needs to be taken with evening meal to increase absorption, but pitavastatin and pravastatin should not be taken near a meal.

42
Q

What three bile acid resins are available?

A

Cholestyramine (Questran, Prevalite), colestipol (Colestid), colesevelam (WelCol)

43
Q

What clinical trial first discovered an increase in blood sugars and potential DM with rosuvastatin therapy?

A

JUPITER

44
Q

What clinical trial lead to the discontinuation of simvastatin 80mg?

A

SEARCH

45
Q

What statins have especially high potential for drug-drug interactions due to CYP 3A4 metabolism?

A

Lovastatin, simvastatin, atorvastatin

46
Q

What is a key sign of rhabdomyolysis? Why is this a cause for concern?

A

Darkened urine–a sign of muscle breakdown and can lead to acute kidney failure!

47
Q

When should LFTs be monitored in statin therapy?

A

At baseline, repeat when clinically indicated.

48
Q

What food should be avoided in statin therapy?

A

Grapefruit/grapefruit juice

49
Q

What patient population should NEVER receive statins?

A

Pregnant women

50
Q

What niche groups is ezetimibe efficaceous for?

A

Patients with CKD, patients recently hospitalized for acute coronary syndrome.

51
Q

What two characteristics may make you use a moderate intensity statin rather than a high intensity statin?

A

Asian ancestry and history of hemorrhagic stroke.

52
Q

What is a key lab marker for muscle breakdown?

A

Creatinine kinase (CK)–D/C statin if 10x ULN

53
Q

What OTC supplement may help prevent statin side effects?

A

Co-Q 150-200mg daily

54
Q

What are the CETP inhibitors (-cetrapib) supposedly especially good at?

A

Elevating HDL (>130% sometimes!)

55
Q

How often should a FLP be monitored on statin therapy?

A

At baseline, at 4-12 weeks following intiiation, and every 3-12 months as indicated. Not as important with new guidelines.

56
Q

What patients should receive CK and AST/ALT monitoring?

A

Patients at higher risk for muscle injury or showing s/sx of myopathy or hepatotoxicity.

57
Q

What three bile acid resins are available?

A

Cholestyramine (Questran, Prevalite), colestipol (Colestid), colesevelam (WelCol)

58
Q

What effects to BARs have on the FLP?

A

Lower LDL and cholesterol, increase TG.

59
Q

What side effects are associated with BARs?

A

GI (constipation, bloating, nausea, flatulence), impaired ADEK absorption, hypernatremia and -chloremia, obstruction

60
Q

What HLD and HTN drugs do BARs alter absorption of?

A

Ezetimibe, fibrates, thiazides.

61
Q

According to the NCEP ATPIII guidelines, are CHD, symptomatic carotid artery disease, PAD, AAA, and DM considered risk equivalents or risk factors?

A

Risk equivalents–risk so high its almost like they already had a heart attack

62
Q

What affect does niacin have on gout, DM, liver problems, and patients on statin therapy?

A

Hyperuricemia, hyperglycemia, increased LFTs, increased level of statins (higher risk for myopathy)

63
Q

What do recent clinical trials say about niacin use?

A

Recently, no reduciton of CV events shown, even though it has beneficial effects on every lipid.

64
Q

What is Vytorin?

A

Ezetimibe + simvastatin

65
Q

What are the groups that may benefit from a statin, but do not necessarily require one?

A

Age 21-39 or >75 with no ASCVD and LDL

66
Q

What side effects are associated with the fibrates?

A

GI upset, rash, myalgia (interacts with statins!), dizziness

67
Q

What are the potential low intensity statin doses? (lower LDL by

A 
Simvastatin 10mg
Pravastatin 10mg or 20mg
Lovastatin 20mg
Fluvastatin 20 or 40mg
Pivatastatin 1mg
68
Q

How are fibrates used clinically?

A

Only to lower triglycerides because they saw no reduction in CV events (except VA-HIT trial).

69
Q

According to NLA, what conditions would classify patients in high risk or very high risk category?

A

DM (high or very high), CKD (high) and clinical ASCVD (very high)–look for these first!

70
Q

How do PCSK9 inhibitors lower LDL?

A

By inhibiting PCSK9, they increase the number of LDL receptors on hepatocytes, which increases the clearance of LDL-C dramatically.

71
Q

What patients would fall into the NLA moderate risk category?

A

2 major ASCVD risk factors but 10-year risk score

72
Q

How is alirocumab (Praluent) dosed? How is evolocumab (Repatha) dosed?

A

Alirocumab: 75mcg SQ q2weeks, may be increased to 150mcg
Evolocumab: 120mcg SQ q2weeks OR 420mcg monthly

73
Q

What is the active ingredient in red yeast rice?

A

Lovastatin

74
Q

What is mipomerson (Kynamro)?

A

An oligonucleotide inhibitor of ApoB-100 synthesis for HoFH–only through REMS, dosed 200mg SQ weekly

75
Q

How does lomitapide (Juxtapid) work?

A

It inhibits triglyceride transfer protein, used in HoFH.

Dosed 5-60mg PO daily

76
Q

Name the 5 risk factors according to ATP III.

A

Smoking, hypertension, low HDL, age (men >45, women >55), FH of premature CHD

77
Q

What are the four statin benefit groups, according to 2013 ACC/AHA?

A 
Clinical ASCVD (includes ACS, MI, angina, arterial revascularization, TIA, PAD)
LDL-C > or = 190 mg/dL
Diabetes and 40-75yo
ASCVD risk > or = 7.5 and 40-75yo
78
Q

What patients would receive a moderate intensity statin in the statin benefit groups?

A

Clinical ASCVD and >75yo

DM and age 40-75yo plus ASCVD or = 7.5% only

79
Q

For what risk categories are drug therapy considered at LDL-C or non-HDL-C levels above treatment goal?

A

Low (+60) and moderate (+30)

80
Q

What are the non-HDL-C, LDL-C and ApoB goals for NLA very high risk patients?

A

Non-HDL-C

81
Q

What are the potential low intensity statin doses? (lower LDL by

A 
Simvastatin 10mg
Pravastatin 10mg or 20mg
Lovastatin 20mg
Fluvastatin 20 or 40mg
Pivatastatin 1mg
82
Q

What are the five major ASCVD risk factors per NLA 2014 guidelines?

A

Age (male >/= 45yo, female >/=55yo)

Family history early CHD (male

83
Q

According to NLA, what conditions would classify patients in high risk or very high risk category?

A

DM, CKD and clinical ASCVD–look for these first!

84
Q

According to NLA, at what TG level can TG be targeted with non-statin medications?

A

500-999: TG lowering agent or statin (if no pancreatitis)

1000+: Fibrates, omega3 fatty acids or niacin

85
Q

What patients would fall into the NLA moderate risk category?

A

2 major ASCVD risk factors but 10-year risk score

86
Q

For a patient with diabetes, what factors would place them in the very high risk category rather than the high risk category according to NLA?

A

Evidence of end-organ damage or 2 or greater major ASCVD risk factors.

87
Q

A patient has an LDL-C of >190. What risk category are they in?

A

High

88
Q

If a patient has two major risk factors and a pooled cohort equation score >15% or framingham >10%, what risk category are they in?

A

High

89
Q

What are the two interchangeable primary targets according to NLA? Secondary target?

A

Primary: Non-HDL-C or LDL-C
Secondary: ApoB

90
Q

What is the non-HDL-C target for patients in NLA risk categories low-high?

A
91
Q

What is the LDL-C target for patients in NLA risk categories low-high?

A
92
Q

What is the ApoB target for patients in NLA risk categories low-high?

A
93
Q

For what risk categories are drug therapy considered at LDL-C or non-HDL-C levels above treatment goal?

A

Low (+60) and moderate (+30)

94
Q

What are the non-HDL-C, LDL-C and ApoB goals for NLA very high risk patients?

A

Non-HDL-C

95
Q

What 3 non-PCOL strategies help control TG?

A

5-10% weight loss
Restriction of alcohol, sugar, refined carbs
Moderate-high intensity physical activity (>150minutes/week)

96
Q

What is a normal triglyceride level? At what level are triglycerides usually treated?

A

Normal: /=500mg/dL

97
Q

Which guideline has specific medicine recommendations for TG management?

A

NLA

98
Q

According to NLA, at what TG level can TG be targeted with non-statin medications?

A

500-999: TG lowering agent or statin (if no pancreatitis)

1000+: Fibrates, omega3 fatty acids or niacin

99
Q

Which guideline addresses ApoB and non-HDL-C goals?

A

NLA–advantage because nonfasting can be used, more predictive

100
Q

Which guideline addresses non-statin therapies?

A

NLA

101
Q

Which guideline relies heavily on the pooled cohort equations to determine risk?

A

ACC/AHA 2013

102
Q

What guideline is targeted to an older patient population and tends to be much less aggressive?

A

VA/DoD guidelines

Pharmacotherapy II (15 decks)

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