Chemistry - Cp Compendium And Osler - Lipids

Front 1

which lipoprotein is the least dense? Most dense?

Back 1

Chylomicrons are least dense (most triglycerides and least protein and lipid). HDL is most dense.

Front 2

What enzyme converts VLDL to IDL?

Back 2

Lipoprotein lipase (LPL). (it is in the muscle and fat and breaks the TG from the VLDL down)

Front 3

What receptors mediate endocytosis of the LDL particle?

Back 3

Apolipoprotein B-100 and LDL receptor

Front 4

What is the function of HDL?

Back 4

To scavenge cholesterol from the periphery and return it to the liver.

Front 5

What is the Friedwald equation?

Back 5

LDL cholesterol = total cholesterol - HDL cholsterol - TG/5

Front 6

What is the friedwald equation not considered valid?

Back 6

If TG>400, if chylomicrons are present, or in type III dyslipidemia

Front 7

What is the major alipoprotein of LDL and VLDLD? What does it do?

Back 7

Apo B. structural. Binds to LDL receptors and also when it binds to liver, the cholesterol released is an inhibitor to the rate limiting step of cholesterol synthesis (HMG coA reductase). It can also bind to scavenger receptors and brings macrophages where we don't want them.

Front 8

What is the major alipoprotein of HDL? what does it do?

Back 8

Apo A1.

It picks up the cholesterol "trash", bags it up (converts it to cholesterol esters) and attaches it to the scavenger receptors on the macrophages.

Front 9

Which Frederickson phenotypes have elevated Tg only?

Back 9

I, IV, V

Front 10

Which Frederickson phenotypes show elevated LDL

Back 10

IIA

Front 11

Which Frederickson phenotypes show elevated Tg and LDL

Back 11

IIB, III

Front 12

What are 2 type I lipid disorders?

Back 12

Familial LPL deficiency, Familial apo C-II deficiency

Front 13

Familial hypercholesterolemia is considered what phenotype?

Back 13

IIa

Front 14

Apolipoprotein E deficiency is considered what phenotype?

Back 14

IIB

Front 15

Familial dysbetalipoproteinemia is considered what phenotype?

Back 15

III

Front 16

Familial hypertriglyeridemia is considered what phenotype?

Back 16

IV, or V

Front 17

Familial combined hyperlipidemia is considered what phenotype?

Back 17

II or IV

Front 18

What are some clinical features of type I lipid disorders?

Back 18

Eruptive xanthomas, pancreatitis

Front 19

What are some clinical features of type IIa lipid disorders?

Back 19

Tendinous xanthomas, premature atherosclerosis

Front 20

According to the ATPIII what are the ranges for cholesterol, (desirable, borderline, high)

Back 20

Desirable <200
Borderline 200-239
High >240

Front 21

According to the ATPIII what are the ranges for LDL?
(Optimal, Near optimal, borderline, high, veryhigh)

Back 21

Optimal <100
Near optimal 100-129
Borderline 130-159
High 160 - 189
Very High >190

Front 22

According to the ATPIII what are the ranges for HDL?

Back 22

Low <40
High >60

Front 23

In type I dyslipidemia, what is the major component of triglycerides?

Back 23

Chylomicrons

Front 24

In type IV dyslipidemia, what is the major component of triglycerides?

Back 24

VLDL

Front 25

In type V dyslipidemia, what is the major component of triglycerides?

Back 25

VLDL and Chylomicrons (think type 1 + 4 = 5)

Front 26

what do chylomicrons do?

Back 26

take TG from intestine to cells that use them (primarily muscle and fat)

Front 27

what does VLDL do?

Back 27

takes endogenously produced TG from liver to muscle and fat.

Front 28

what is LDL and what does it do?

Back 28

LDL is a metabolic byproduct of metabolism of VLDL. It delivers cholesterol.

Front 29

what is apo-CII?

Back 29

co factor for LPL.

from Osler: tries to metabolize TG on "trucks". It leaves liver on HDL truck. In circulation, it jumps onto truck that has TG. Stands in the back of truck and tosses TG out to LPL. So, it helps LPL work.

Front 30

What is Apo-E?

Back 30

surface in VLDL, chylo; involved in receptor binding, remnant release

from Osler: it is the remote control over the garage that allows empty trucks inside. So...these truck remnants are going to the liver to be metabolized.

Front 31

what are three variants of apoprotein E?

Back 31

E3 - has just right amount of binding to receptors. Most common.

E2 - doesn't really bind to receptors. So, causes high IDL

E4- too sticky. binds onto receptors and doesn't let go. Also, binds onto other stuff (i.e. amyloid - link to Alzheimers)

Front 32

what is special about apoprotein a?

Back 32

sticky on both ends. On one side, binds to apoB so it can stick onto LDL particles. The other end looks like plasmin and it can bind fibrin. So, there is increased atherosclerosis and thrombosis if there is an increased Lp(a).

Front 33

what are small dense LDL?

Back 33

very efficient way of getting rid of their cholesterol and depositing it in body. So, increased risk of atherosclerosis.

Front 34

what is phospholipase A2?

Back 34

enzyme produced by macrophages, in blood,, associated with the LDL molecule. Appears to oxidize lipid in LDL, producing inflammatory lipids. Localized to atherosclerotic plaques. Increaes risk of occlusive events, especially stroke.

Front 35

what is specifically measured when measuring triglyceride?

Back 35

glycerol

Front 36

what is the purpose of the glycerol blank?

Back 36

measure glycerol twice. Once before they add LPL and once after. Then subtract amount present before from the total.