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Clin Med Exam 1(Lauren) > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Where does most cholesterol come from?

A

Made in liver

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2
Q

Is atherosclerosis a TYPE of arteriosclerosis (hardening of arteries)?

A

Yes

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3
Q

What are the “Ubers” of lipids?

A

Lipoproteins

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4
Q

What causes atherosclerosis?

A

Abnormal lipoprotein metabolism

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5
Q

What usually causes abnormal lipoprotein metabolism?

A

Genetics!!! (Not diet)

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6
Q

What are the 5 types of lipoproteins?

A

Chylomicrons

VLDL

IDL

LDL

HDL

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7
Q

What do chylomicrons do?

A

Carry dietary lipids from the intestine to the liver and rest of the body

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8
Q

What do VLDLs do?

A

Carry newly made triglycerides from liver to adipose

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9
Q

What do LDLs do?

A

Carry CHOLESTEROL from liver to the rest of the body

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10
Q

What do HDLs do?

A

Collect cholesterol from the rest of the body (including the vascular endothelium 😀) and return it to the liver for excretion

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11
Q

Does the action of HDLs provide a protective effect against heart disease?

A

Yes

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12
Q

What should you suspect in anyone with a family history of premature atherosclerotic cardiovascular disease (ASCVD)?

A

An inherited increased lipid disorder

(Familial hypercholesterolemia
Polygenic hypercholesterolemia
Familial combined hyperlipidemia)

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13
Q

What are the 3 types of inherited increased lipid disorders discussed in class?

A

Familial hypercholesterolemia

Polygenic hypercholesterolemia

Familial combined hyperlipidemia

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14
Q

Is familial hypercholesterolemia monogenic or polygenic?

A

Monogenic

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15
Q

How often does familial hypercholesterolemia occur?

A

1 in a million

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16
Q

What are the 2 forms of familial hypercholesterolemia?

A

Heterozygotes- 2x normal LDL

Homozygous- 8x normal LDL

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17
Q

How do you treat familial hypercholesterolemia?

A

Statin, and consider add-on

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18
Q

How do you treat polygenic hypercholesterolemia?

A

Statin, consider add-on

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19
Q

How common is familial combined hyperlipidemia?

A

1-2% of general population

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20
Q

How do you treat familial combined hyperlipidemia?

A

Statin

Second agent if needed

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21
Q

Is familial combined hyperlipidemia monogenic or polygenic?

A

Polygenic

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22
Q

What is secondary hyperlipidema?

A

Hyperlipidemia with a NON-lipid etiology

Ex: diabetes, alcoholism, diet, smoking, obesity, hypothyroidism, CKD, liver disease, drugs (steroids)

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23
Q

Which is more common: inherited hyperlipidemia or secondary hyperlipidemia?

A

Inherited

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24
Q

What are the 4 steps to atherosclerosis?

A
  1. LDL molecules diffuse through the endothelium at a rate DEPENDENT on concentration of LDL in blood
  2. Macrophages follow, absorb LDL, and become foam cells. Then they die, release cholesterol, and form deposits
  3. Body reacts with increased collagen to form a cap
  4. Cap ruptures and thrombus forms, leading to potential infarct
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25
Q

When does UpToDate recommend we screen for familial hyperlipidemia?

A

Before puberty (9-11 yrs) and

After puberty (17-21 yrs)

(However, there is no established interval. The decision to screen should be based on overal risk of coronary heart disease independent of lipid levels)

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26
Q

What are the non-modifiable risk factors for coronary heart disease?

A

Family history of premature ASCVD

Age (men over 45, women over 55)

Male gender

Symptomatic cardiovascular disease

Chronic kidney disease

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27
Q

What are the modifiable risk factors for coronary heart disease?

A

Hyperlipidemia**

HDL less than 40**

HTN (BP 140/90 or on HTN drugs)

Diabetes

Tobacco

Obesity

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28
Q

What level of HDL is a negative risk factor for CHD?

A

60 or higher

HDL IS GOOD

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29
Q

What is measured in a fasting lipid panel?

A

Total cholesterol

Triglycerides

LDL

HDL

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30
Q

How do you calculate total cholesterol?

A

HDL+LDL+ (triglycerides/5)

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31
Q

How long should you fast before doing a fasting lipid panel, and why?

A

12 hours

Triglycerides are greatly affected by eating, although cholesterol is not

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32
Q

Acutely ill patient may have falsely (high/low) levels in a lipid panel

A

Low

Cholesterol levels can drop 24-48 hours after a heart attack and can persist for up to 60 days

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33
Q

Your patient had a heart attack yesterday and when you checked his fasting lipid panel today, everything was really low! WTF?!

A

Cholesterol levels drop after a heart attack and may persist for up to 60 days

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34
Q

What is a desirable cholesterol level?

A

Under 200

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35
Q

What is a borderline cholesterol level?

A

200-239

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36
Q

What is a high risk cholesterol level

A

240+

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37
Q

What is a desirable triglyceride level?

A

Under 150

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38
Q

What is a borderline triglyceride level?

A

150-199

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39
Q

What is a high risk triglyceride level?

A

200-499

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40
Q

What is a desirable HDL?

A

60+

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41
Q

What is a borderline HDL?

A

35-45

42
Q

What is a high risk HDL?

A

Under 35

43
Q

What is a desirable LDL?

A

60-130

44
Q

What is a borderline LDL?

A

130-159

45
Q

What is a high risk LDL?

A

160-189

46
Q

What are plane xanthomas?

A

Cholesterol-filled, soft yellow plaques that appear in various places (eyelids, palmar creases, etc)

47
Q

What type of hypercholesterolemias do plane xanthomas indicate?

A

Familial OR secondary causes

48
Q

What are tuberous xanthomas?

A

Yellow-orange nodules often located on knees, elbows, and tendons

49
Q

What kind of hypercholesterolemia are tuberous xanthomas associated with?

A

Familial

50
Q

Do eruptive xanthomas happen over time or suddenly all at once?

A

Suddenly all at once in response to extremely high triglycerides (often over 1500mg)

51
Q

What do eruptive xanthomas look like and where do they show up?

A

Crops of small red and yellow papules that are most common on buttcheeks and extensor surfaces

52
Q

What type of hyperlipidemia do eruptive xanthomas indicate?

A

Familial HLD

53
Q

What is a corneal Arcus?

A

A white or grey ring around the cornea that may be caused by high cholesterol

54
Q

Is a corneal arcus abnormal all the time?

A

No, it can be normal in pts over 40

55
Q

What is the best diet to manage lipids?

A

DASH diet (Dietary Approaches to Stop HTN)

  • lots of fruits and veggies
  • moderate amounts of low-fat dairy
  • low animal protein
  • lots of plant protein like nuts and legumes
  • low sodium
56
Q

Can exercise actually increase HDL cholesterol?

A

Why yes it can

57
Q

What is the only class of drugs to demonstrate clear inmprovements in overall mortality in preventing heart attacks?

A

Statins

58
Q

What class of drugs is the focus of the Joint National Committee’s 8 recommendations?

A

Statins

59
Q

What enzyme is inhibited by statins?

A

HMG-CoA reductase (an enzyme that makes cholesterol in the liver)

60
Q

As a result of statins inhibiting HMG-CoA reductase and inhibiting cholesterol synthesis, what happens next?

A

Blood cholesterol levels decrease.

Liver enzymes sense that cholesterol production has decreased, so they increase production of LDL receptors.

Receptors relocate to the liver cell membranes and bind to passing LDL and VLDL.

LDL and VLDL enter the liver and are digested.

61
Q

What are the adverse effects of statins?

A
  • mild GI complaints
  • liver toxicity
  • muscle pain
  • rhabdomyolysis
62
Q

When should a patient take their statin?

A

At bedtime (most cholesterol is produced at night)

63
Q

What are the ABSOLUTE contraindications of statins?

A

Active liver disease

Pregnancy

64
Q

In which patients should you use statins “with caution?”

A

Concomitant use of CYP3A4 inhibitors

Chronic kidney/liver disease

65
Q

What are the 2 types of statin regimens?

A

High-Intensity

Moderate-Intensity

66
Q

What labs do you need to draw before you start a pt on statins?

A

Baseline lipid panel

Liver function tests

Creatine kinase

67
Q

After starting statins, how often should you check their lipid panel?

A

6-8 weeks after starting

Every 6-12 months thereafter

68
Q

How do bile acid sequestrants (resins) work?

A

Bind bile acids in the intestine and prevent reabsorption

Decreases LDL

(May actually increase triglycerides)

69
Q

Are bile acid sequestrants/resins safe during pregnancy?

A

Yes

70
Q

How do Bile acid sequestrants (resins) interact with statins?

A

Synergistically

71
Q

What are the adverse effects of bile acid sequestrants (resins)?

A

Constipation

Farting

Inhibit fat soluble vitamin absorption

Might affect Warfarin

Can increase triglycerides!!!**

72
Q

What are the contraindications to bile acid sequestrants/resins?

A

Absolute: Triglycerides over 400

Relative: Triglycerides over 200

73
Q

What 3 drugs are bile acid sequestrants/resins?

A

Cholestyramine

Colesevelam

Colestipol

(They affect CHOLESTerol in your COLon)

74
Q

What is the effect of Nicotinic Acid/Niacin?

A

Reduces production of LDL

Increases HDL

May reduce triglycerides

75
Q

What are the adverse effects of Nicotinic acid/niacin?

A

Flushing and itching**

Liver damage**

May be unsafe when used with statin

76
Q

What are the absolute and relative contraindications to Nicotinic acid/niacin?

A

Absolute: Active liver disease

Relative:
hyperuricemia

Hyperglycemia

Unstable angina

77
Q

Is Nicotinic acid/niacin safe to use during pregnancy?

A

NO

78
Q

What are the 3 drugs that are Fibric Acid Derivatives?

A

Gemfibrozil

Fenofibrate

Bezafibrate

79
Q

What is the best class of drug for lowering triglycerides

A

Fibric acid derivatives

May lower TGs up to 50%

80
Q

In addition to lowering the fuck out of your triglycerides, can fibric acid derivatives increase your HDL too?

A

Yes, up to 25%

81
Q

Do we give fibric acid derivatives to pregnant women?

A

No

82
Q

What are the adverse effects of fibric acid derivatives?

A

Gallstones

Hepatitis

Myositis

83
Q

What are the absolute and relative contraindications to fibric acid derivatives?

A

Absolute:
Gallstones
Taking Simvastatin**
Severe liver/kidney disease

Relative:
Other statin use (risk of myopathy)
On Warfarin

84
Q

Your patient is taking simvastatin. What class of drugs must he absolutely avoid?

A

Fibric acid derivatives

Gemfibrozil, fenofibrate, bezafibrate

85
Q

How does ezetimibe/zetia work?

A

Blocks intestinal absorption of dietary and biliary cholesterol

86
Q

Can you use ezetamibe/Zetia with a statin?

A

Yes

87
Q

What are the contraindications to ezetamibe/zetia?

A

Pregnancy

Using it with a statin in someone with liver disease***

88
Q

What effect does Ezetamibe/Zetia have on your lipid panel?

A

Lowers LDL

89
Q

If your patient is on a statin and you suspect they have myositis (rhabdo), what should you do?

A

Stop statin and check CK level

90
Q

What effect do PCSK9 Inhibitors have on your lipid panel?

A

Lower LDL

91
Q

Do we know a lot about PCSK9 inhibitors?

A

No, it is a very new and expensive injection

92
Q

According to the JNC 8 Recommendations, what should the goal of hyperlipidemia treatment be?

A

ASCVD risk reduction

NOT target lipid levels

93
Q

According the JNC 8 Recommendations, should we give statins to everyone?

A

No, only in those who are most likely to benefit

94
Q

What are the 4 statin benefit groups?

A
  1. People with clinical ASCVD (angina, MI, strokes, TIAs, acute coronary syndromes)
  2. People with LDL levels 190+
  3. 40-75 year old diabetics
  4. 10 year ASCVD risk is 7.5% or higher according to the Pooled Cohort calculator
95
Q

What type of therapy should people in Group 1 get?

A

High intensity statin

BUT if they’re older than 75, do moderate-intensity statin

96
Q

What type of therapy should people in group 2 get?

A

High intensity statin

97
Q

What type of therapy should people in group 3 get?

A

Moderate intensity statin

BUT if the calculator said they were over 7.5%, you should do a High-intensity statin

98
Q

What type of therapy should someone in group 4 get?

A

Moderate to high intensity statin

99
Q

What are some of the other factors you might take into consideration if someone is not in groups 1-4, and the benefit of statin therapy is unclear?

A

LDL=160 or higher

Family history of premature ASCVD

Hs-CRP = 2 or higher

ABI < 0.9

Elevated lifetime risk of ASCVD according to calculator

100
Q

What is the MOST important contributor to the ASCVD risk calculation?

A

Age

101
Q

Should you just prescribe statins to everyone and never ask the patient what he thinks?

A

No, your treatment plan should be a comprehensive approach to risk reduction that incorporates addressing modifiable risk factors and assessing ASCVD risk with the calculator

Clin Med Exam 1(Lauren) (8 decks)

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