Atherosclerosis, HDL and LDL

Question 1

What is the normal use of Cholesterol in the body?

Answer 1

• synthesis and repair of cell membranes and organelles

- precursor to steroid hormones

Question 2

What is the normal use of Triglycerides in the body?

Answer 2

fuel source for muscle use and adipose tissue storage

Question 3

What protein is critical for the metabolism of lipoproteins?

Answer 3

Apoprotein

Question 4

VLDL is mostly composed of what?

Answer 4

Triglycerides

Question 5

Chylomicrons are mostly composed of what?

Answer 5

triglycerides

Question 6

what does exogenous lipid metabolism mean?

Answer 6

metabolism of fat which is from dietary intake. as opposed to endogenous lipid metabolism which takes care of fat produced from your liver.

Question 7

Describe exogenous fat ingestion.

Answer 7

dietary fat is ingested–>in the intestine it becomes a chylomicron–>LPL takes the triglycerides out of chylomicron and uses them for storage or skeletal muscle etc.
–>After TGs are gone chylomicron is now chylomicron remnant–> remnant binds to remnant receptor on liver for further metabolism.

Question 8

Describe exogenous metabolism.

Answer 8

liver produces VLDL–> LPL take TGs out of VLDL to use in body–> with TGs removed VLDL becomes IDL–>LPL converts IDL to LDL–> LDL binds LDL receptor on liver.

Question 9

What is the role of PCSK9?

Answer 9

it prevents the LDL receptor from arising on liver and thus slows down lipid metabolism. There is a drug to inhibit PCSK9.

Question 10

A patient who is fasting should have no circulating _______.

Answer 10

chylomicrons

Question 11

Why is HDL beneficial in lipid metabolism?

Answer 11

can clear cholesterol out of the system by a route other than liver receptors.

Question 12

what is the key elevated factor that leads to atherosclerosis (and coronary heart disease risk)?

Answer 12

LDL-C

Question 13

Describe the pathophys of atherosclerosis.

Answer 13

circulating LDL is taken up into the subendothelial space. Gets oxidized there (this is one reason why anti-oxidants are a good thing). It releases pro-inflammatory cytokines. Monocytes go in there next and eat the LDL. These monocytes (macrophages) now turn into foam cells because they ate tons of fat. Foam cells and T-cells within the plaque cause MMP secretion and activation of tissue factors. Eventually you get accumulation of these cells which can turn into an atheroma. An atheroma in the subendothelial space is what can eventually rupture (if unstable) and lead to vessel thrombosis.

Question 14

Whats the difference between minimal, moderate, and severe atherosclerosis?

Answer 14

in minimal and moderate we see compensatory expansion of the blood vessel to keep lumen the right size. In severe, the compensatory mechanism is overcome and the lumen narrows.

Question 15

Whats the difference between a vulnerable and a stable plaque? How do you stabilize a plaque?

Answer 15

a vulnerable plaque has a thin fibrous cap and is subject to rupture.

Lower cholesterol.

Question 16

What are the different atherogenic lipoproteins? Why are these important.

Answer 16

LDL, VLDL, IDL, remnants.

They are central to the initiation and progression of atherosclerosis

Question 17

Adults ____ y/o and older should have a lipid panel done every 5 years.

Answer 17

20.

Question 18

the process of cholesterol leading to atherosclerosis happens fast and at any age.

Answer 18

false. it is a slow progressive process that likely starts at a young age.

Question 19

How do risk factors in a patient correlate with LDL-C goals? what are the specific numbers?

Answer 19

1 RF– goal LDL-C level

Question 20

what is the formula to determine lipoprotein levels.

Answer 20

LDL=total cholesterol- HDL - (TG/5)

This might not be that important but its a good way to think about it.

note: TG/5 only works when TGs

Question 21

What are the four major Statin benefit groups?

Answer 21

1. individuals with known clinical ASCVD
2. individuals with LDL >/=190
3. individuals with diabetes
4. individuals without diabetes but who have an estimated 10-year ASCVD risk >/= 7.5%

Question 22

How does calcium relate to risk for ASCVD?

Answer 22

elevated coronary calcium suggests elevated risk of atherosclerosis

Question 23

Severe hypertriglyceridemia is probably a risk factor for ASCVD, right? So we should probably lower them right?

Answer 23

welllllll, it is a risk factor for ASCVD but its unclear if lowering it actually helps.

its also a risk factor for acute pancreatitis

Question 24

A low HDL _____ your risk for CV disease regardless of LDL levels.

Answer 24

increases.

However, we’re not sure if raising HDL-C actually helps, just like not sure if lowering TGs actually helps.

Question 25

Men or women are at higher risk for CVD?

Answer 25

men… until over 80, then more women are at risk (probably because the men that should be in this category are dead by then).

Question 26

CVD is the leading cause of death in our society. At what age group is it the most serious?

Answer 26

under 85 CVD=cancer in deaths. Over 85 CVD is the leading cause of death.