Lipids

Question 1

What are the main reasons to assess lipids?

Answer 1

1. diagnose lipid/lipoprotein metabolism disorders
2. Diagnose lipid storage disorders/mitochondrial oxidation disorders
3. cardiovascular risk assessment

Question 2

ON THE TEST: WHat were the data points used in the traditional framingham risk score?

Answer 2

age, gender, smoking status, total cholesterol, HDL, systolic BP and HTN Rx

Question 3

Where do most patients fall in the framingham risk score? Why is this an issue?

Answer 3

76% fell in the low risk category, but people in this category still had CV events

Question 4

What do we use now instead of framingham?

Answer 4

the 2013 ACC/AHA guidelines, which has new pooled cohort equations for ASCVD risk assessment with different equations for nonwhite populations

Question 5

Statin therapy is recommended in what 4 groups under the ACC/AHA guidelines?

Answer 5

1. Diabetics
2. LDL > 190
3. ASCVD risk > 7.5% with LDL 70-189
4. Secondary prevention in other high risk groups ??

Question 6

True or false: the ACC/AHA guidelines have no LDL or non-HDL treatment targets

Answer 6

true

Question 7

What risk factors are taken into account for the ACC/AHA ASCVD risk calculator?

Answer 7

sex, age, race, total chol, HDL, SBP, BP treatment, Diabetes, Smoker status

Question 8

What are the 6 major classes of lipoproteins?

Answer 8

chylomicrons
VLDL
IDL
LDL
HDL
Liproprotein A

Question 9

Which lipoprotein particle is the causal agent in atherosclerosis?

Answer 9

LDL particle - the more LDL a person has, the higher the risk for plaque buildup

Question 10

Is LDL cholesterol and LDL particle?

Answer 10

No - LDL cholesterol is just the cholesterol that makes up the LDL particle. As such, it’s not a perfect measure of LDL and LDL_attributable risk

Question 11

Reduction in LDL cholesterol by 40 mg/dL reduces CHD risk by ___%

Answer 11

20%

Question 12

What is the optimal LDL liprotein level?

Answer 12

50-70 mg/DL

There is NO atherosclerosis progression at LDL-C < 67 mg/dL

Question 13

ON THE TEST: What equation is the most common method for reporting LDL?

Answer 13

The Friedewald equation, which assumes al cholesterol is VLDL, LDL and HDL

cLDL = [Tot Chol] - [HDL chol] - [Tg]/5

Question 14

When should the Friedewald equation not be used?

Answer 14

when the TG > 400 because it assumed chylomicrons, IDL and liporpotein A are not signficant, but if you have a TG > 400, you definitely have some chylomicrons floating around

Question 15

If someone does have elevated TGs, what is a better number to use for risk prediction beyond the LDL-C?

Answer 15

the non-HDL-c

Question 16

What are the two primary reasons to perform lipid screening in pediatrics?

Answer 16

1. identify childhood dyslipidemia (in pediatric obesity and T2DM)
2. ID genetic hyperlipidemia (with fam hx of early CV)

note: we can differentiate normal lipids from abnormal lipid by age 2

Question 17

Describe familial hypercholesterolemia.

Answer 17

an inheritable, AD disorder of mutation in the LDL receptor; resulting in severe hypercholesterolemia present starting in chldhood with CVD early in life

one of the most commonly occurring genetic disorders (1:200 to 500)

Question 18

What LDL level would you expect with a heterozyote FH? Homozygote?

Answer 18

hetero > 190

Homo > 600-1000

Question 19

How can cholesterol testing be used to make a phenotypic diagnosis of FH?

Answer 19

> 190 makes it likely
160 with positive family hx
135 with positive genetic dx in family

Question 20

What secondary causes should be ruled out before you move to genetic testing for FH

Answer 20

thyroid disease
liver disease
renal disease
medication effect
obesity

Question 21

Ideally, when should you screen for discrimination of FH?

Answer 21

in childhood! Lipid screening is most effective in early childhood (ages 1-9)

Question 22

Should we universally screen all children ages 1-9 then?

Answer 22

Hard to say. Some organizations say yes. USPSTF says inconclusive.

If strong family hx of early CV or physical findings of FH in the child, consider screening as early as age 2

Question 23

In adult HF patients, what is the treatment titration goal?

Answer 23

get an LDL-C reduction of at least 50% from baseline

Question 24

What is the treatment strategy to get to this goal?

Answer 24

start with mod to high statin monotherapy

then add ezetimibe

then add things like bile acid sequestrants, fibrates, nicotinic acids

apheresis is last resort for treatment in heterozygous FH, but actually a first-line therapy in homozygous FH because it won’t respond to drugs or lifestyle modifications

Question 25

ON THE TEST: Apo-A1 is associated which which lipoproteins? Functioning as what?

Answer 25

HDL - part of HDL structure

Chylomicrons: LCAT ativator

Question 26

ON THE TEST: Apo-B100 is associated with what lipoproteins? Functioning as what?

Answer 26

VLDL, IDL, LDL

It binds the LDL receptor and is part of structure for all three

Question 27

ON THE TEST: ApoB48 is associated with which lipoprotein? Function?

Answer 27

Chylomicron - structural

Question 28

ON THE TEST: What are the two most common hyperlipidemia phenotype in the US?

Answer 28

IV (45%)

IIb (40%)

Question 29

ON THE TEST: Describe phenotype I. WHat’s elevated?

Answer 29

Mainly chylomicrons

so plasma cholesterol level is up, triglycerid level is waaay up

Question 30

ON THE TEST: Describe phenotype IIa. What’s up?

Answer 30

LDL is up

so plasma cholesterol is high but TGs are normal. very high athero-genicity

Question 31

ON THE TEST: Describe phenotype IIb. What’s up?

Answer 31

LDL and VLDL

so high cholesterol, high TGs and high athero-genicity

Question 32

ON THE TEST: Describe phenotype III. WHat’s up?

Answer 32

IDL

high cholesterol and very high TGs; high ahtero-genicity

Question 33

ON THE TEST: Describe phenotype IV. What’s up?

Answer 33

VLDL

normal to high plasma cholesterol. mildly elevated TGs. relatively low athero-genicity

Question 34

ON THE TEST: Describe phenotype V. What’s up?

Answer 34

VLDL and chylomicrons

so mildly increased cholesterol, very high TGs. relatively low athero-genicity

Question 35

What phenotype is familial hypercholesterolemia?

Answer 35

IIa