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Clin Med Cardio Exam 2 > Dyslipidemias > Flashcards

Dyslipidemias Flashcards

1
Q

Thickened and hardened lesions of the medium and large muscular and elastic arteries that are lipid rich

A

Atherosclerosis

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2
Q

Carries lipid to the arteries (must be oxidized)

A

LDL

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3
Q

Removes lipid from the arteries

A

HDL

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4
Q

What is the major source of endogenously derived cholesterol?

A

Liver and intestines

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5
Q

Where do you exogenously derive cholesterol?

A

Diet

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6
Q

What is the rate limiting step in the liver for cholesterol biosynthesis?

A

Converting HMG CoA to mevalonic acid by HMG CoA reductase

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7
Q

If you increase your intake of dietary cholesterol, what happens?

A

Down regulation of LDL receptors leads to subsequent elevation of serum LDL cholesterol

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8
Q

What can lead to the uptake of lipoproteins?

A

Vascular injury (smoking, HTN, DM)

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9
Q

Elevation of ____ can directly lead to vascular injury resulting in premature atherosclerosis

A

LDL (oxidized)

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10
Q

What is necessary for LDL to damage endothelial cells?

A

Oxidation

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11
Q

The relation between serum HDL and atherosclerosis is ____

A

Inverse

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12
Q

If your patient has normal LDL, but has low HDL, does this put them at risk for CHD?

A

Yes!

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13
Q

Clinical findings of hyperlipidemia

A 
Often asymptomatic 
Atherosclerosis
Eruptive xanthomas
Tendinous xanthomas
Xanthelasma
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14
Q

Most cases of adult dyslipidemia are ____

A

Multifactoral - diet, lifestyle, genes

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15
Q

Which diseases put you at risk for dyslipidemias?

A

DM, renal failure, hypothyroidism

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16
Q

What causes familial hypercholesterolemia?

A

LDL recepter defect (heterozygous)

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17
Q

What is the goal of treatment in secondary prevention of CHD?

A

To prevent recurrent coronary events and decrease coronary and total mortality (Prevention from progressing)

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18
Q

Patients with known CHD have a known incidence of ____X risk of MI

A

5-7

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19
Q

What are the 4 key groups for statin therapy?

A
  1. ASCVD history
  2. Primary elevation of LDL greater than or equal to 190mg/dL
  3. 45-70 y.o. with diabetes, and LDL from 70-189 w/o ASCVD
  4. 45-70 y.o. without clinical ASCVD or diabetes with LDL 70-189 with 10 year ASCVD risk of 7.5 or higher
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20
Q

Are there goals based on specific LDL values?

A

No! No evidence to support

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21
Q

Which therapies are HIGH intensity daily doses that lower LDL cholesterol? How much do they lower it by?

A

Atorvastatin, Rousuvastatin

50%

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22
Q

Which therapies are MODERATE intensity daily doses that lower LDL cholesterol? How much do they lower it by?

A

Simvastatin, Pravastatin, Lovastatin

30%

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23
Q

Who should receive high intensity statins?

A

All patients with ASCVD unless they are not a candidate and patients with LDL greater than 190 mg/dL

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24
Q

Diabetics with a 10 year ASCVD risk greater than 7.5 should receive??

A

High intensity statins

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25
Q

Diabetics with a 10 year ASCVD risk lower than 7.5 should receive?

A

Moderate intensity statins

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26
Q

Patients 40-75 years with a 10 year ASCVD risk greater than 7.5 should receive?

A

Moderate to high intensity statins

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27
Q

What is the NNT that you need to treat with Atorvastatin to prevent one MI, one stroke, etc.

A

25

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28
Q

How do you prevent atherosclerosis?

A

LOWER LDL!!

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29
Q

How do you treat an individual who is younger than 40?

A

Use clinical judgement - cause other cholesterol lowering agents may be considered in addition to statins

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30
Q

What is the optimal value of total cholesterol? HDL?

A

170mg/dL total

50g/dL HDL

31
Q

Does having high triglycerides put you at an increased risk for CAD/CHD?

A

Not necessarily - more risk when LDL is high or HDL is low

32
Q

How are VLDL and HDL related?

33
Q

What do high triglycerides put you at risk for?

A

Pancreatitis

34
Q

Should you treat hypertriglyceridemia?

A

Yes, but lowering LDL is more important!

35
Q

Hypertriglyceridemia is very sensitive to ??

A

Diet, weight reduction, and exercise

36
Q

If your patients triglycerides are greater than 200mg/dL, should you treat them?

A

Yes! Also consider Rx if HDL is very low!

37
Q

How do you treat hypertriglyceridemia?

A

Fabric acid agents or niacin

38
Q

Why is HDL good?

A

It is cardioprotective and directly protective

39
Q

What does HDL do?

A

Facilitates removal of cholesterol in tissues

40
Q

What non-pharmacologic treatments can increase HDL?

A

Weight loss, regular exercise, smoking cessation, estrogen therapy in post menopausal women (avoid where possible), decrease alcohol intake

41
Q

What meds can increase HDL?

A

Fibric acid and niacin – drugs used to treat hypertriglyceridemia

42
Q

Do drugs that raise HDL reduce CV events and endpoints?

43
Q

Why do drugs that raise HDL not help with endpoints?

A

It is raising the cholesterol HDL carries, but not the particles or proteins within the HDL molecule

44
Q

What is the most important part of the HDL molecule that makes it anti-atherogenic?

A

The particles

45
Q

The ideal diet is less than ____% fat, ____% saturated fat ____mg/day cholesterol

A

should be less than 30% fat, 7% saturated fat, and less than 200mg/day cholesterol

46
Q

How should you replace fats in the diet?

A

Carbohydrates or monosaturated fatty acids

47
Q

MOA of statins?

A

HMG CoA reductase inhibitors

48
Q

Inhibit rate limiting step in cholesterol synthesis in liver; up regulate synthesis of LDL receptors - further reduction LDL cholesterol; LDL and TC lowered by 30-55%

49
Q

What is the most commonly reported adverse effect of statins

A

Statin myopathy

50
Q

What is the most common statin myopathy?

A

Myalgias

CK will most likely be normal

51
Q

What is a rare but life threatening type of statin myopathy? What will be increased with this condition?

A

Myositis with rhabdomyolysis

CK will be increased 10X upper limit of normal

If present, DC drug!

52
Q

If your patient complains of a statin myopathy, what should you do?

A
  1. Stop/hold drug immediately
  2. Get CK
  3. If CK is not elevated or mildly elevated then you just decrease the dose of statin
53
Q

What increases the risk of statin myopathy?

A

Increased with drugs that inhibit statin metabolism

54
Q

What is a major endocrine issue with statin therapy?

A

Can cause chemical diabetes

55
Q

Who is at risk for chemical diabetes?

A
  1. HTN
  2. Obesity
  3. FBG greater than 100
  4. TG greater than 150
56
Q

Does the decrease of CV events while taking statins outweigh the risk of chemical diabetes?

57
Q

What are some added benefits of statins?

A
  1. Plaque stabilization
  2. Anti-inflammatory effects
  3. Reduce CRP levels
  4. Protection of vessels subject to invasive coronary interventions
58
Q

What is more effective at lowering LDL levels and decreasing CV events than doubling the dose of a statin?

A

Adding Ezetimibe plus a low/moderate dose of statin

59
Q

When ezetimibe is added to a statin, how much additional LDL is lowered?

A

25%! Holy shet

60
Q

For patients with heterozygous familial hypercholesterolemia or patients with ASCVD already taking max doses of statin

A

Alirocumab

61
Q

Bind bile in the intestine and stimulate conversion of cholesterol to bile acids in the liver; up regulate LDL receptors- result is decrease in LDL cholesterol

A

Bile acid sequestrants

62
Q

Decreases VLDL synthesis and release, lowers triglycerides to a lesser degree than LDL cholesterol, and RAISES HDL

A

Nicotinic acid

63
Q

What is important when dosing nicotinic acid to avoid side effects of flushing/itching and GI symptoms?

A

Start with a very low dose and work upwards

64
Q

What is the primary effect of fabric acid derivtatives like gemfibrozil and fenofibrate?

A

Lower triglycerides; mild reduction of LDL-C

65
Q

Outline the guidelines for drug therapy for elevated LDL and total cholesterol

A
  1. Statin
  2. If unable to use statin use nonstatin (ezetimibe, cholestyramine, etc.)
  3. Add other agents to a statin on a case by case basis
66
Q

Outline the guidelines for drug therapy for elevated triglycerides and hypercholesterolemia

A
  1. Lifestyle change is very very important!
  2. If diet and exercise don’t work consider Rx: gemfibrozil, fenofibrate, or niacin
  3. If LDL remains above goal, add statin
67
Q

What enzyme binds to LDL receptors on hepatocytes, promoting receptor degradation, preventing LDL-C clearance from blood and is associated with familial hypercholesterolemia

68
Q

What type of drug is Alirocumab

A

PCSK9 inhibitor

69
Q

What is the problem with bile acid sequestriants?

A

Lots of GI side effects

70
Q

What does VLDL carry?

A

Triglycerides

71
Q

When will you see eruptive xanthomas? (Red papules on buttock)

A

Very high triglycerides (VLDL)

72
Q

When will you see tendinous xanthomas (nodules on tendons)?

A

Very high LDL

73
Q

What is the best way to reduce mortality and morbidity from coronary heart disease?

A

Diet and drug induced reductions of LDL

74
Q

Which drugs inhibit statin metabolism?

A

Niacin, fibrates, bile acid sequestrants, ketoconazole, erythromycin, clarithromycin, cyclosporins

Clin Med Cardio Exam 2 (6 decks)

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