Dyslipidemia and CVD part 1

Question 1

hypolipoproteinemias 3 examples

Answer 1

1. abetalipoproteinemia

2. familial hypobetalipoproteinemia 3. tangier disease ( alpha-lipoprotein deficiency )

Question 2

abetalipoproteinemia

Answer 2

defect in app B synth

- no chiylo, VLDL, LDL and TG accumulate in the liver and intestine

Question 3

familial hypobetalipoproteinemia

Answer 3

LDL concentration is 10-50% of normal but chill formation occurs

Question 4

tangier disease

Answer 4

absence of HDL, CE accumulate in tissues, chill, VLDL, LDL all normal,

Question 5

most common hyperlipoproteinemia phenotypes

Answer 5

IIb (LDL and VLDL- mutation of LDL receptor and app B) and IV (VLDL)- but no marker

Question 6

majority of genotype for apo-E

Answer 6

60% have E-3/E-3

Question 7

what’s the bad one of apo-E

Answer 7

E-2/E-2 bc it does not bind to the LDL receptor so increased VLDL

Question 8

primary dyslipidemia classification?

Answer 8

single or poly-genetic abnormality affecting lipoprotein function resulting in hyper to hip lipidemia

Question 9

type 1 - hyperchylomicronemia

Answer 9

high TG, low HDL, skin xANTHOMAS, PANCREATITIS,

Question 10

type IIa- hypercholesterolemia

Answer 10

high LDL and Tg normal or high,

symptoms: xanthekasma, vascular disease

Question 11

type IIb- combined hyperlipoproteinemia

Answer 11

high LDL and VLDL and high apo-B

serum: high chol, high TG and low HDL

Question 12

type III- dysbetalipoproteinemia

Answer 12

high b-VLDL IDL

and high LDL and VLDL

Question 13

type IV- hypertriglyceridem a

Answer 13

high VLDL

Question 14

type V- mixed hyperlipidemia

Answer 14

high VLDL, and CM

Question 15

Total CH

Answer 15

less than 5.2mmol/L

Question 16

HDL levels

Answer 16

want more than 1.0 men

more than 1.3 in women

Question 17

LDL levels

Answer 17

want less than 2.6

Question 18

TG levels

Answer 18

want less than 1.7

Question 19

apoproteins

Answer 19

primary determinant of the metabolic fate of lipoproteins

Question 20

VLDL major apoproteins

Answer 20

B-100 and E and C

Question 21

LDL major apoprotein

Answer 21

B-100

Question 22

HDL major apoprotein

Answer 22

A1, AII, C, E

Question 23

CM major apoproteins

Answer 23

B-48, E, A1, AIV, C11, C111

Question 24

Apo e-2 does not bind to

Answer 24

LDL receptor ( so higher VLDL ruminants)

Question 25

defect in app B synth ( no CM, VLDL, LDL formed and TG accumulate in liver and intestine

Answer 25

abetalipoproteinemia

Question 26

LDL is 10-15% of normal but CM still occurs

Answer 26

familial hypobetalipoprotinemia

Question 27

Tangier disease

Answer 27

absence of HDL - no apo A-II - can't take away CE from tissues ( so accumulate) CM, VLDL, LDL are normal

Question 28

which hyperlipidemias have the greatest CVD risk? why?

Answer 28

IIb ( combined hyperlipoprotinemia) and III dysbetalipoproteinemia) - bc high in both LDL and VLDL

Question 29

hyperchylomicronemia

Answer 29

no CVD risk | this is when there is low LPL so CM accumulatie, leading to high TG and low HDL

Question 30

Hypercholesterolemia

Answer 30

polygenic- affecting LDL receptors and means that there are higher levels of LDL-C circulating but normal TG ( or high) ( + CVD risk)

Question 31

combined hyperlipoproteinemia

Answer 31

+++ CVD risk - mutation in LDL receptor or APO B such that there is high LDL and VLDL ( so high CE and high TG with low HDL)

Question 32

dys-beta-lipo-protein-emia

Answer 32

E2/E2

Question 33

high TG and VLDL ?

Answer 33

IV- hypertriglyceridemia

Question 34

in type V- why is there a white band at the top?

Answer 34

``` CM floating ( the least dense) - this is mixed hyperlipidemia ( with high VLDL - like in hypertriglyceridemia) but this one is different bc also has high CM ```

Question 35

when will blood look more white?

Answer 35

when there is accumulation of TG from CM or VLDL

Question 36

why does IIA ( hypercholesterolemia look normal?

Answer 36

high CH, from LDL but TG are normal

Question 37

what are some medications that can cause secondary dyslipidemia?

Answer 37

thiazide diuretics, B- blockers, corticosteroids, estrogens,

Question 38

HSL role in obesity and lipoprotein metabolism

Answer 38

activity is increased bc high adipose tissue and if insulin resistance there is a lot of insulin being produced levels - end result is increased substrate flux to the liver

Question 39

describe the effect of alcohol on VLDL levels

Answer 39

ethanol blocks the pathway of acyl-CoA to oxidation ( for energy) so more acetyl-CoA will get converted to TG and get packaged in VLDL - more VLDL, more lipolysis, more TG uptake into tissues ( fat deposit)

Question 40

effect of obesity on lipoprotein metabolism

Answer 40

over production of VLDL, increased lipolysis ( normal levels of VLDL but higher fat deposit)

Question 41

how does hyper-triglyceremia happen with obesity?

Answer 41

``` VLDL defect. lipolytic effect (high TG if high VLDL) ```

Question 42

how would hyper-cholesterolemia come from obesity?

Answer 42

LDL - if there was a defect in the LDL receptor - a diet very high in sat fats

Question 43

posible mechanism for reduced HDL in obesity?

Answer 43

CE get transferred to VLDL and HDL takes up a TG, when this happens excessively, increased catabolism of HDL bc lots more adipose tissue

Question 44

2 factors associated with low HDL in obesity?

Answer 44

severity (BMI) - inverse relationship between HDL ( this is a stronger affect than the effect of raised LDL and obesity) and distribution ( abdominal)

Question 45

what casues the decrease in HDL in obesity?

Answer 45

enhanced uptake of HDL2 by adipocytes and and increase in catabolism of apolipoprotein A-1

Question 46

who should be screened?

Answer 46

all mena nd women over the age of 40 | - abdominal aortic aneurysm, obesity, Diabetes, hypertension, family history of premature CVD

Question 47

FRS

Answer 47

is a test that estimates your 10-year cardiovascular disease risk we use this information to stratify the risk - so if FRS is above20% high risk, if between 10-19% intermediate risk

Question 48

when does FRS double?

Answer 48

if person is aged 30-55 without diabetes and has a relative with premature CVD

Question 49

which are the 5 statin indicated conditions

Answer 49

1. atherosclerosis, 2.diabetes, 3.chronic kidney disease, 4.abdominal aortic aneurysm 5. LDL more than 5mmol/L

Question 50

CVD intermediate risk ?

Answer 50

FRS of 10-19% LDL > 3.5 ( should be under 2.6) non-HDL > 4.3 or men or women with one of more psi factor that are one the age of 50 ( men and 60 women)

Question 51

what 2 methods as alternatives for LDL

Answer 51

non-HDL-C and apo-B as alternative targets

Question 52

primary target for high risk (>20% FRS)

Answer 52

<2.0 LDL

Question 53

primary target if intermediate risk and LDL is greater that 3.5?

Answer 53

<2.0 LDL

Question 54

primary target if low risk but LDL is greater than 5.0 so we initiate treatment ( <10% FRS)

Answer 54

>50% decrease in LDL-C