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Boards And Beyond > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

LDL less than ….. is very good

A

100 mg/dl

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2
Q

LDL more than ….. is high

A

200 mg/dl

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3
Q

HDL less than ……. mg/dl is low

A

45

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4
Q

HDL does not necessarily decrease chances or risks for atherogenesis but low HDL increases risk
True or false

A

True

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5
Q

What is the normal TG level

A

<150mg/dl

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6
Q

TG greater than 1000mg/dl can cause which condition

A

Pancreatitis

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7
Q

Elevated TG levels is only modestly associated with CAD. Little evidence that lowering high levels reduces risk for atherogenesis
True or false

A

True

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8
Q

Lowering TG levels is not mostly for treating CAD or lowering risk but rather for lowering risk of what condition

A

Pancreatitis

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9
Q

What is hyperlipidemia

A

Elevated total cholesterol, LDL or TGs
It’s a risk factor for coronary disease and stroke

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10
Q

What are some lifestyle factors which could increase risk of hyperlipidemia

A

Sedentary lifestyle
Saturated and trans-fatty acid foods
Lack of fiber

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11
Q

What is primary hyperlipidemia

A

The cause of the hyperlipidemia is by elevation of LDLs, TGs and TCs and not any other underlying or secondary cause

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12
Q

What are some causes of secondary hyperlipidemia

A

Alcohol
Pregnancy (provides more lipids for the baby)
Beta-blockers
HCTZ (thiazide diuretics)
Thyroid disease
Nephrotic syndrome

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13
Q

What are the treatments for hyperlipidemia

A

Recommend lifestyle modification (healthy diet, weight loss, quit smoking)
Statin therapy

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14
Q

What are the two types of therapy for statins

A

Moderate-intensity statins
High-intensity statins

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15
Q

What are some choices for moderate intensity statin therapy

A

Atorvastatin 10 to 20 mg/day
Rosuvastatin 5 to 10 mg/day
Simvastatin 20 to 40 mg/day

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16
Q

What are some choices for high intensity statin therapy

A

Atorvastatin 40 to 80 mg/day
Rosuvastatin 20 to 40 mg/day

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17
Q

What is the maximum dose for Atorvastatin

A

80 mg/day

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18
Q

What is the maximum dose for Rosuvastatin

A

40 mg/day

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19
Q

What is the treatment goal for hyperlipidemia

A

To get the LDL under a 100mg/dL
For patients with known vascular disease, the goal is often to get them under 70mg/dL

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20
Q

When should you put a patient on a high intensity stain therapy

A

Patient with CAD, stroke or PAD
Patient with LDL > 190 mg/dL

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21
Q

When should you put a patient on a moderate or high intensity statin therapy

A

Diabetics greater than 40 years old
ASCVD risk greater than 7.5% over 10 years

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22
Q

What are some signs of hyperlipidemia

A

Most patients have no signs and symptoms
Screen patients with blood tests
Physical findings occur in patients (xanthomas, tendinous xanthoma, corneal arcus) with severe high lipids (they usually have a genetic familial syndrome)

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23
Q

What are xanthomas

A

They are plaques of lipid-laden cells
They appear as skin bumps or on eyelids

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24
Q

What is a tendinous xanthoma

A

Lipid deposits in tendons
Common in Achilles

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25
Q

What is a corneal arcus

A

Lipid deposits in cornea
Looks like a ring around the iris

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26
Q

Which familial dyslipidemias are autosomal recessive (AR)

A

Types I and III

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27
Q

Which familial dyslipidemias are autosomal dominant (AD)

A

IIa and IV

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28
Q

What is another name for type I dyslipidemia

A

Hyperchylomicronemia

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29
Q

People with hyperchylomicronemia could have elevated triglycerides greater than ……… mg/dL

A

1000

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30
Q

What plasma appearance is characteristic of type I dyslipidemia

A

Milky plasma appearance

31
Q

What is the main problem people have with type I dyslipidemia

A

Recurrent pancreatitis
Enlarged liver and xanthomas might also be present

32
Q

What is the mainstay treatment for people with type I dyslipidemia

A

Very low-fat diet

33
Q

Type I dyslipidemia is associated with what enzyme dysfunction

A

LPL (lipoprotein lipase)

34
Q

There is no apparent risk in which familial dyslipidemia

A

Type I dyslipidemia

35
Q

Which is another name for type II dyslipidemia

A

Familial hypercholesterolemia

36
Q

In which type of familial dyslipidemia do people have few or zero LDL receptors to pull LDL from plasma into the liver thus leading to very high LDL levels

A

Type II dyslipidemia

Patient can develop tendinous xanthomas and corneal arcus

37
Q

What is the main problem in type II dyslipidemias

A

Severe atherosclerosis (can have MI in their 20s)

38
Q

Which familial dyslipidemia is caused by mutations in the apo E gene

A

Type III Dyslipidemia

39
Q

What is another name for type III dyslipidemia

A

Familial dysbetalipoproteinemia

40
Q

In which familial dyslipidemia are there accumulations of beta lipoproteins

A

Type III dyslipidemia

41
Q

Chylomicron remnants and VLDLs are collectively called

A

Beta lipoproteins

42
Q

In which familial dyslipidemia are beta lipoproteins poorly cleared by the liver

A

Type III dyslipidemia

43
Q

In which familial dyslipidemia are both TC and TG levels elevated
(TC elevation usually mild. TC > 300 mg/dL)

A

Type III dyslipidemia

44
Q

In which familial dyslipidemia could you have a premature coronary disease

A

Type III dyslipidemia

45
Q

What is another name for type IV dyslipidemia

A

Hypertriglyceridemia

46
Q

In which familial dyslipidemia is there VLDL overproduction or impaired catabolism of VLDLs

A

Type IV dyslipidemia

47
Q

Which familial dyslipidemia is associated with type II diabetes and hypertension

A

Type IV dyslipidemia

48
Q

What are some lipid lowering therapies

A

Statins
Niacin
Fibrates
Absorption blockers
Bile acid resins
PCSK9 inhibitors
Omega-3 fatty acids

49
Q

Which lipid lowering therapy inhibits HMG CoA reductase

A

Statins

50
Q

What are the MOA of statins

A

Low cholesterol synthesis in the liver which then increase LDL receptors in the liver to pull in plasma cholesterol
Major effect: LDL decrease

51
Q

Mention some statins

A

Atorvastatin
Simvastatin
Lovastatin

52
Q

Which lipid lowering therapy could cause:
Hepatotoxity (rise in AST/ALT)
Muscle problems

A

Statins

53
Q

What is the most common muscle problem associated with statins

A

Myalgia (patients complain of weakness and soreness but if you measure serum CK levels to look for evidence of muscle damage, it would be normal)

54
Q

What is a less common but more serious muscle problem associated with statins

A

Myositis (inflammation of the muscles)
(symptoms similar to myalgias, but CK levels are increased in the serum)

55
Q

What are some statin muscle problems

A

Myalgias
Myositis
Rhabdomyolysis

56
Q

What is a very rare but much more serious statin muscle problem

A

Rhabdomyolysis
(weakness, muscle pain, dark urine from myoglobin spilling into plasma and the urine, serum CK levels very high-1000 or more, acute renal failure -> death)

Rhabdomyolysis rarely occurs just from taking a statin, it usually occurs when someone takes a statin in conjunction with another drug. Eg. Genfibrozil, P450 inhibitors)

57
Q

What are the three main statins that are metabolized by the P450 system

A

Atorvastatin
Simvastatin
Lovastatin

58
Q

Mention some statins which are not metabolized by the P450 system

A

Ravastatin
Rosuvastatin

59
Q

Mention some P450 inhibitors which should not be taken together with some statins

A

Cyclosporine
Macrolide antibiotics
Azole antifungal agents
HIV protease inhibitors
Grapefruit juice

60
Q

What is the effect of P450 inhibitors on statins

A

P450 metabolizes statins. Thus, taking a P450 inhibitor would increase plasma levels of statins which could cause myalgias, rhabdomyolysis, etc

61
Q

Mention one supplement (vitamin) which could be used in the treatment of hyperlipidemia by administering high doses

A

Niacin

LDL will fall and increases HDL

62
Q

Which drug in the treatment of hyperlipidemia could cause flushing (stimulates PGs in the skin, face turns red and warm, effect fades with time)

A

Niacin

63
Q

What drug could you take to blunt the side effect of flushing by niacin

A

Aspirin (inhibits prostaglandins)

64
Q

Which supplement used in the treatment of hyperlipidemia should be avoided in diabetic patients because it leads to hyperglycemia and hyperuricemia (thus can precipitate a gout attack)

A

Niacin

65
Q

What is the commonly used drug for patients with high levels of TGs

A

Fibrates

66
Q

Give some examples of fibrates

A

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

67
Q

Which drug works by activating PPAR-a thus increasing LPL activity leading the liver to break down more fatty acids (fatty acid oxidation)

A

Fibrates

68
Q

What kind of fibrate is rather used when a patient is to be on both a statin and dictate together

A

Fenofibrate
Don’t use gemfibrozil

69
Q

Which drug could raise LFTs thus increase cholesterol gallstones and cause myositis

A

Fibrates

70
Q

Mention one cholesterol absorption blocker

A

Ezetimibe

71
Q

Which of the lipid curing therapies is highly selective for cholesterol and thus does not affect fat-soluble vitamins and TGs

A

Cholesterol absorption blockers

72
Q

Where is the worksite for cholesterol absorption blockers

A

Intestinal brush border

73
Q

Why are use of statins picked over absorption blockers

A

Weak data on hard outcomes (MI, death) for absorption blockers

74
Q

Which lipid curing drug could cause diarrhea

A

Absorption blockers

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