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Cardiovascular > Atherosclerosis, HDL, and LDL > Flashcards

Atherosclerosis, HDL, and LDL Flashcards

1
Q

What 2 things are cholesterol normally for?

A
  1. Synthesis and repair of cell membranes and organelles
  2. Precursor of steroid hormones

(but you don’t need a whole lot of cholesterol to do these things)

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2
Q

What are triglycerides normally for?

A

Fuel source for muscle use and adipose tissue storage

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3
Q

What is the generic lipoprotein structure?

A

On the inside, you have triglycerides and cholesterol esters. On the outside, you have a hydrophilic polar coat made up of phospholipids, a little cholesterol, and apoproteins.

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4
Q

Lipids are _____ so they won’t freely circulate around the blood stream. This is why they need to be packaged into _____ structures.

A

hydrophobic, lipoprotein

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5
Q

Why are apoproteins important?

A

They determine the metabolism of the lipoproteins.

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6
Q

While all lipoproteins are spherical, they do differ in _____.

A

Density

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7
Q

Chylomicrons are the ______ of lipoproteins and come from _____ and are mainly made of _____.

A

Least dense, Diet, triglycerides

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8
Q

VLDL are similar to _____ in that they are mainly made of _____.

A

Chylomicrons, triglycerides

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9
Q

List the lipoproteins from most dense to least dense

A

HDL, LDL, VLDL, Chylomicrons

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10
Q

VLDL is produced by the _____.

A

Liver

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11
Q

Liver produces triglycerides in the form of _____.

A

VLDL

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12
Q

VLDL eventually gets metabolized into ____.

A

LDL

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13
Q

LDL is mainly made of ____

A

cholesterol

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14
Q

HDL is 40% ____, 30% _____, and 27% _____.

A

(Generally) 40% protein, 30% phospholipids, 27% cholesterol

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15
Q

Explain the physiology of exogenous lipid metabolism

A

Dietary fat is absorbed through GI tract. Within the GI cells, you package the triglyceride and a little bit of cholesterol into a Chylomicron. Chylomicrons then get dumped into the lymph system and then go into the vascular system. LPL (lipoprotein lipase) takes the triglycerides from chylomicrons and stores it into cells (e.g. skeletal muscle or fat). After the triglyceride is taken from the chylomicron, you are left with a chylomicron remnant (denser). This remnant is taken up by the liver via a remnant receptor.

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16
Q

Chylomicrons have 3 key proteins. What are they?

A

Apoprotein E, C-2, B-48

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17
Q

Which apoprotein helps chylomicrons bind to LPL enzyme?

A

C-2

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18
Q

How do we measure a patient’s endogenous lipid metabolism?

A

Patient needs to fast for 8-12 hours so that the lipid panel shows only endogenous activity.

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19
Q

Explain the physiology of endogenous lipid metabolism

A

Liver produces VLDL. As VLDL circulates in the blood stream, LPL (lipoprotein lipase) takes the triglycerides from chylomicrons and stores it into cells (e.g. skeletal muscle or fat). After the triglyceride is taken from the VLDL, you are left with IDL (a denser remnant). Eventually, more triglycerides are removed from IDL (by LPL) and you get LDL (even more dense). LDL is eventually taken up by LDL receptors on the liver. The LDL is taken by the receptor into the liver cell where it can be used and the receptor resurfaces so it can grab more LDL.

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20
Q

VLDLs have 3 key proteins. What are they?

A

Apoprotein C-2, E, B-100

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21
Q

Which apoprotein helps LDL bind to the liver LDL receptors?

A

Apoprotein B-100

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22
Q

What is protein PCSK9? What are protein PCSK9 inhibitors?

A

PCSK9 protein binds to the LDL receptor on the liver preventing it from resurfacing. When the LDL receptor brings LDL into the liver cell, protein PCSK9 prevents the receptor from going back to the surface. So, it’s harder to clear LDL because the number of working receptors is diminished because of PCSK9. We have drugs that inhibit PCSK9 so that we have more LDL receptors to clear more LDL from the blood stream.

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23
Q

What is nascent HDL?

A

It’s HDL without lipids in it… it just has phospholipids and protein

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24
Q

What is LCAT enzyme?

A

Lecithin-cholesterol acyltransferase accepts cholesterol into the nascent HDL turning it into mature HDL.

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25
Q

What is CETP enzyme?

A

Cholesterol ester transfer protein. It is the enzyme that allows mature HDL to transfer VLDL/LDL.

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26
Q

Why does Mature HDL transfer VLDL/LDL?

A

Mature HDL takes VLDL/LDL cholesterol from the circulation and from cells and clears it from the system (this way doesn’t involve LDL receptor). This is thought to be good because you’re clearing more cholesterol from the system.

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27
Q

In addition to clearing VLDL/LDL, 2 other benefits of HDL are…

A

Anti-inflammatory and anti-oxidant (this helps prevent atherosclerosis)

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28
Q

LDL cholesterol elevations lead to ______

A

atherosclerosis

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29
Q

LDL cholesterol elevations are associated with an increase risk of _____

A

CAD

30
Q

True or False: LDL cholesterol lowering reduces heart disease related events and deaths

A

True

31
Q

What are the steps for atherosclerosis and plaque pathogenesis?

A

Circulating LDL is taken up into sub endothelial space. In this space, it gets oxidized. Oxidized LDL releases factors that attract monocytes. Monocytes turn into macrophages and eat the LDL and turn into foam cells. Foam cells accumulate and you have the process of atherosclerosis. Without LDL, you don’t get this process.

32
Q

Why are anti-oxidants potentially good?

A

They can reduce the amount of oxidized LDL

33
Q

When LDL gets into the sub endothelial space, it is oxidized and glycosylated. This releases a lot of pro inflammatory molecules. Name 7 of them.

A
  1. TNFalpha (tumor necrosis factor alpha)
  2. IL-1 (interleukin-1)
  3. IL-6
  4. IFN (interferons)
  5. Cell adhesion molecules (CAMs)
  6. Monocyte chemotactic protein-1 (MCP-1)
  7. IL-8
34
Q

Foam cells and T-lymphocytes within plaques cause _____ secretion and ____ of tissue factors.

A

Matrix metalloproteinase (MMP), activation

35
Q

Name the atherogenic lipoprotein(s)

A

LDL, VLDL, IDL, remnants. We usually consider LDL to be the main culprit but the other ones are actually also considered to be atherogenic lipoproteins and are all central to the initiation and progression of atherosclerosis.

36
Q

True or False: Atherosclerosis ignition and progression is a slow and progressive process likely starting at a young age.

A

True

37
Q

At what age and time intervals is it recommended for having fasting lipid panels done?

A

Adults 20 y/o and older at least every 5 years. Complete lipoprotein profile after 8-12 hour fast.

38
Q

In Complete lipoprotein profile, what is the main lipoprotein of interest?

A

LDL

39
Q

How do you measure LDL?

A

It’s calculated using Friedewald formula which is better than any direct measurement of LDL.

In fasted state,
Total cholesterol = LDL + HDL + VLDL
VLDL = TG/5 when TG are less than 400 mg/dl
Therefore:
LDL = Total Cholesterol - HDL - (TG/5)
40
Q

What’s normal LDL-C?

A

It’s hard to determine what normal LDL is. For a long time, we have risk stratified so patients with higher risk should really try to keep their LDL lower and patients with lower risk factors are acceptable to have a little elevation in LDL. However, recent studies have shown that these stratifications don’t help.

41
Q

What is average LDL-C in USA?

A

130 mg/dl (although this is likely elevated from what’s physiologically normal since we are born with ~30 mg/dl)

42
Q

True or false: The majority of CHD occurs with “average” cholesterol

A

True

43
Q

True or false: CHD can/does occur with “low” cholesterol

A

True

44
Q

What are the 4 risk groups that should be treated aggressively with statins?

A
  1. Individuals with known clinical ASCVD
  2. Individuals with LDL > 190 mg/dl (severe hypercholesterolemia. often familial conditions)
  3. Individuals with diabetes (>40 y/o and LDL >70)
  4. Individuals (>40 y/o, LDL >70) without ASCVD or diabetes who have an estimated 10-year ASCVD risk >7.5%
45
Q

What are the 9 risk factors for ASCVD?

A
  1. Sex
  2. Age
  3. Race
  4. Total cholesterol (untreated)
  5. HDL
  6. Systolic BP (current)
  7. Treatment for HTN (y/n)
  8. Diabetes
  9. Smoking
46
Q

What is premature ASCVD?

A

ASCVD event before age of 55 (men) or 65 (women). Women are protected until after menopause.

47
Q

What is hsCRP?

A

Highly sensitive C-reactive protein. This is a lab test for systemic inflammation.

48
Q

If a patient whose 10-year risk is “moderate” (5-7.5%), or when the decision is unclear, what other factors may be used to enhance the treatment decision making? (there are 5)

A
  1. Family history of premature ASCVD
  2. LDL-C >160 mg/dl
  3. hsCRP > 2 mg/dl
  4. Coronary Calcium Score >300 Agatston units or >75th percentile for age, sex, ethnicity
  5. Ankle-Brachial Index
49
Q

What is coronary calcium score?

A

This tests for calcium in coronary arteries. Calcium suggests atherosclerosis. It can’t tell if the plaques are stable or unstable but if you have a score over 300 or over 75th percentile for age, sex, ethnicity, this may be an indication that the patient needs to be put on statins.

50
Q

What are the 4 lifestyle modifications recommended to treat ASCVD risk in adults?

A
  1. Heart healthy diet (aim for 5-6% saturated fat and low trans fat, emphasize fresh vegetables/fruits, whole grains, low-fat dairy, poultry, fish, legumes, nuts, vegetable oils, low sodium intake especially in HTN)
  2. Regular exercise
  3. Avoidance of tobacco
  4. Maintain healthy weight
51
Q

Most ASCVD patients on statins should be on ____ or _____ intensity statins.

A

High, moderate

52
Q

Name the 2 high-intensity statin dosages

A

Atorvastatin (40)80 mg, rosuvastatin 20(40) mg

53
Q

Name 8 moderate-intensity statins dosages

A 
Atorvastatin 10(20) mg
Rosuvastatin (5)10 mg
Simvastatin 20-40 mg
Pravastatin 40(80) mg
Lovastatin 40 mg
Fluvastatin XL 80 mg
Fluvastatin 40 mg BID
Pitavastatin 2-4 mg
54
Q

How much does a daily dose of high-intensity statin reduce LDL-C by?

A

> 50%

55
Q

How much does a daily dose of moderate-intensity statin reduce LDL-C by?

A

30-50%

56
Q

How much does daily dose of low-intensity statin therapy reduce LDL-C by?

A
57
Q

Name 5 low-intensity statin therapy dosages

A 
Simvastatin 10 mg
Pravastatin 10-20 mg
Lovastatin 20 mg
Flavastatin 20-40 mg
Pitavastatin 1 mg
58
Q

What are three tests to rule out secondary causes of dyslipidemia?

A
  1. TSH (e.g. to rule out hypothyroidism)
  2. UA (e.g. to rule out nephrotic syndromes)
  3. LFT(e.g. to rule out biliary liver disease)
59
Q

Smoking cessation causes about %____ drop in 10 year ASCVD risk

A

%50

60
Q

Why is there still such high residual risk (50-70%) in patients treated with statins? (2 theories)

A
  1. Maybe we are treating patients too late. By the time they are started on statins, there has already been significant atherosclerosis formed.
  2. Maybe we haven’t lowered LDL enough. With new drugs like the PCSK9 inhibitors, perhaps we can lower the LDLs even better reduction in cardiac events.
61
Q

What does a blood draw from a hypertriglyceridemia patient look like?

A

It is full of lipid. “lipemic serum”

62
Q

What is the main health risk for severe hypertriglyceridemia patients?

A

Acute Pancreatitis (can be fatal)

63
Q

Are severe hypertriglyceridemia patients prone to MIs and strokes?

A

No, the main concern is acute pancreatitis

64
Q

What is the health risk for moderate hypertriglyceridemia patients?

A

ASCVD. It is shown that moderate hypertriglyceridemia is associated with higher risk for ASCVD but it is unclear whether or not lowering triglycerides is beneficial. Hypertriglyceridemia is associated with insulin resistance, metabolic syndrome, and type 2 diabetes which makes it unclear if hypertriglyceridemia is just associated with ASCVD or actually causing it.

65
Q

What causes hypertriglyceridemia?

A

Genetic + secondary causes. (thyroid disease, alcohol, drugs, uncontrolled diabetes, estrogens, etc)

66
Q

The _____ the HDL, the _____ the risk for CAD

A

lower, higher

67
Q

What are 3 properties of HDL that potentially make it a positive thing?

A
  1. reverse transport of LDL
  2. Anti-inflammatory
  3. Anti-oxidant
68
Q

True or false: There is evidence that HDL raising reduces ASCVD related events/death

A

False

69
Q

True or false: There is evidence that low HDL levels are associated with increased risk for ASCVD and high HDL levels are associated with protective effect against ASCVD.

A

True

70
Q

What medication is given to raise HDL? (But has no shown clinical benefit)

A

CETP inhibitors

71
Q

What are side effects of statins?

A

Increased risk of MSK aches and pains. (5-15% of patients).

Myositis (?) - Extremely rare (inflammation of muscle leading to severe levels of CPK)

72
Q

What do you do if a patient doesn’t tolerate a particular statin drug?

A

Put the patient on other statin drugs until you find one that they will tolerate. This usually works. Or try different dosing patterns. Sometimes statins that a patient couldn’t tolerate 10 years ago, all of the sudden they are okay with that statin. Mechanisms are unclear..

Cardiovascular (22 decks)

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