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Clin for Final > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

0
Q

What new discovery was found in the Framingham study?

A

That there was two different types of cholesterol, and that as HDL goes down the higher risk for heart disease.

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1
Q

What is a commonality between the Japanese and French diet?

A

Relatively low GI, high fruit and veg, less red meat, fish.

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2
Q

What is a general intake as fat intake increases?

A

Increase antioxidant intake to counter any proxidants effects.

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3
Q

What factors increase HDL levels?

A

Saturated fats, dietary cholesterol, alcohol, exercise, estrogens, female gender.

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4
Q

What factors decrease HDL?

A

Simple sugars/high CHO, polyunsaturated fat, high androgens, anabolic steroids, some antihypertensive drugs, obesity, DM, cigarette smoking, physical inactivity, male gender.

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5
Q

What are the potentially controllable risk factors for heart disease?

A

Elevated blood fats, high blood pressure, smoking, excess body fat, lack of exercise, stress

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6
Q

What lifestyle interventions work at the genotypic LDL level?

A

Diet, obesity, stress.

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7
Q

What lifestyle interventions work at the phenotypic LDL level (elevated)?

A

Hypertension + diabetes control! HDL level, stress, smoking.

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8
Q

What lifestyle interventions work at the coronary artery disease level?

A

Physical activity, smoking, stress.

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9
Q

Describe the first theory of coronary artery disease.

A

Endothelial-injury hypothesis that endothelial injury leads to the adherence of platelets and release of platelet derived growth factor which leads to cell proliferation and an advanced lesion.

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10
Q

Describe the second theory of coronary artery disease.

A

Lipid-infiltration hypothesis. High plasma LDL level leads to LDL infiltration and more oxidized LDL, which leads to the formation of foam cells and a fatty streak.

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11
Q

Describe the third theory of coronary artery disease.

A

Obesity as a state of inflammation, inflammation causes problems in the liver with the transport of all fats and at the level of the endothelial walls.

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12
Q

What are probable causes of “initiation” (arterial injury)?

A

Lipid oxidation products, smoking, hypertension.

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13
Q

What are probable causes of “progression” (atherosclerotic plaque)?

A

High LDL, high oxidized LDL.

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14
Q

What are probably causes of “termination” (myocardial infarction)?

A

Low omega 3, high omega 6, high lipid oxidation products.

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15
Q

What is the main component of chylomicrons?

A

Triglycerides.

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16
Q

What is the main component of VLDL?

A

Triglycerides.

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17
Q

What is the main component of LDL?

A

Cholesterol esters.

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18
Q

What is the main component of HDL?

A

Proteins and phospholipids.

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19
Q

What are the main functions of apoproteins?

A

Stabilize surface, activate enzymes, interact with cell surface receptors.

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20
Q

A patient has survived an MI. What apoproteins levels would have have expected to see before the MI?

A

Low A, high B

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21
Q

What are the major apoproteins of chylomicrons?

A

A1, A4
B (48 for liver)
C (lipoprotein lipase), E ->both from HDL

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22
Q

What major apoproteins are in VLDL?

A

B100
C (lipoprotein lipase)
E

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23
Q

What major apoproteins are in LDL?

A

B100

24
Q

What major apoproteins are in HDL?

A

A1, A2

Also carries apoproteins to transfer to other lipoproteins.

25
Q

Why is the E2 genotype not desirable?

A

E2 does not have a very high binding affinity for the Apo-E LDL receptor of the liver. Will see higher LDL levels because not bring tracked to the liver effectively.

26
Q

Describe abetalipoproteinemia.

A

Defect in Apo-B. Can’t form chylomicrons, VLDL, or LDL. TAG accumulates in the liver and interferes with function. Poor absorption of fats from the gut.

27
Q

Describe familial hypobetalipoproteinemia.

A

LDL concentration is 10-50% of normal, but chylomicrons formation still occurs.

28
Q

Describe familial-alpha lipoprotein deficiency (Tangier disease).

A

Virtual absence of HDL. Levels of chylomicrons, VLDL, and LDL are all normal. Will have hyper triglycerides because the absence of Apo C, which is needed for lipoprotein lipase.

29
Q

What are some clinical features of hypercholesterolemia (phenotype 2a)?

A

Vascular disease, xanthomas.

30
Q

What are some clinical features of combined hyperlipidemia (phenotype 2b)?

A

Glucose intolerance, xanthomas, Etoh intake

31
Q

What are some clinical features of endogenous hyprrtroglyceridemia (phenotype 4)?

A

Glucose intolerance, excess Etoh

32
Q

How is LDL calculated?

A

LDL=total chol- HDL - TG/5
Only valid if TG less than 4.5 mmolL
Units: mg/dL

33
Q

For 30+ and no other risk factors what is the optimal total cholesterol level and what action should be taken?

A

Below 200 mg/dL. Reevaluate lipid risk factors as part of periodic health examination.

34
Q

For 30+ and no other risk factors what is a borderline high total cholesterol level and what action should be taken?

A

200-240. Treat if: LDL >130, HDL <35, or trig >200.

Treat with dietary modifications. If insufficient, treat with drug therapy.

35
Q

For 30+ and no other risk factors what is considered high for total cholesterol and what action should be taken?

A

>

  1. Treat with dietary modifications, if not sufficient add drug therapy.
36
Q

For adults with other risk factors, what action should be taken?

A

Tx may be initiated at lower levels of total and LDL cholesterol.

37
Q

For adults 18-29 with no other risk factors what is considered optimal and what action should be taken?

A

<180. Reevaluate as part of periodic health examination.

38
Q

For adults 18-29 with no other risk factors what is considered borderline high and what action should be taken?

A

180-200. Treat if: LDL >115, HDL<35, TG >200. Treat with dietary interventions, drugs if not sufficient.

39
Q

For adults 18-29 with no other risk factors what is considered high for overall cholesterol and what action should be taken?

A

>

  1. Treat with diet, drugs if not sufficient.
40
Q

What is the conversion factor for total serum cholesterol from mg/dL to mmol/L?

A

0.02586

41
Q

What is the conversion factor for total serum triglyceride from mg/dL to mmol/L?

A

0.01129

42
Q

What path creates the hypertriglyceridemia of obesity?

A

Overproduction of VLDL-TGs (high free fatty acids, high carbs)
Lipolytic effect backs up so have a build up of VLDL. Insulin resistance and glycated LPL contributes to.

43
Q

What path contributes to the hypercholesterolemia of obesity?

A

Overproduction of VLDL (from high caloric intake)

Reduced activity of the LDL receptor (high saturated fats, cholesterol contributes to)

44
Q

How much cholesterol is lost through fecal matter everyday?

A

About 0.5 g

45
Q

Where can Apo-E be added to VLDL?

A

In the liver, gut, or plasma.

46
Q

How does alcohol effect lipid processing in the hepatic cells?

A

Inhibits oxidation of acetylcho-A, so increase fatty acid production in the liver.

47
Q

Obesity increases endogenous cholesterol synthesis by ________ per kg of excess body weight.

A

20 mg/day

48
Q

What is a possible mechanism for the lowering of HDL by obesity?

A

Increased catabolism of HDL by excess adiposith. Sequester HDL in fat stores.

49
Q

What receptor in the liver recognizes chylomicrons? IDL/LDL?

A

B48
B100/E
LDL can also enter by a non receptor mediated pathway!

50
Q

What effects are there on a hepatic cell if the free cholesterol pool is very high?

A

Inhibits endogenous synthesis of cholesterol, down regulates LDL receptors, stimulates ACAT (converts cholesterol to cholesterol esters).

51
Q

What a Apo proteins does HDL carry a reserve of?

A

A, C, E

52
Q

What apoproteins are added to chylomicrons by HDL? What apoproteins were already present on nascent chylomicrons? What apoproteins are recycled to HDL?

A

C, E. B48, A. A, C.

53
Q

What apoproteins does VLDL get from HDL? What did it already have in nascent state? What does is recycle to HDL?

A

C, E. B100, A. C.

54
Q

What apoproteins are on IDL? LDL?

A

B100, E. B100.

55
Q

Where is HDL synthesized?

A

Liver and small intestine.

56
Q

By what enzyme and cofactor does HDL pick up cholesterol from tissues?

A

A1 and LCAT

57
Q

What enzyme allows chylomicrons and VLDL to give HDL it’s triglycerides, and VLDL to pick up the cholesterol?

A

CETP

58
Q

How do the triglycerides return to the liver?

A

HRHL (HTGL)

Clin for Final (5 decks)

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