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Drew 922 > 4_2cholesterol > Flashcards

4_2cholesterol Flashcards

1
Q

What is the active form of HCR?

A

dephosphorylated (insulin)

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2
Q

How is HCR regulated?

A

feedback (transcription repression by cholesterol and bile) and phosphorylation (de-PO4 = active)

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3
Q

What causes statin side effects?

A

synthesis of HMG-CoA when cholesterol is low

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4
Q

Where is most cholesterol synthesized?

A

liver/intestine

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5
Q

dietary sources of cholesterol

A

egg yolk, red meat, liver

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6
Q

What diseases is cholesterol correlated with?

A

CVD, stroke

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7
Q

What are the characteristics of cholesterol’s structure?

A

1) 27 C; 2) 3’ S-beta-up OH; 3) 5-6 ene; 4) 8C side chain; 5) 3 6-membered and 1 5-membered ring

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8
Q

What are the effects of bile acid sequestrants alone?

A

reduce cholesterol up to 20%

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9
Q

What are the effects of bile acid sequestrants in combo with a statin?

A

55% reduction

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10
Q

Is ezetimibe natural or synthetic?

A

natural

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11
Q

What is the mechanism of ezetimibe?

A

binds to NPC1L1 in brush border

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12
Q

What are ADRs of ezetimibe?

A

growth of plaques in arteries; HA, diarrhea

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13
Q

statin ADRs?

A

dementia, inhibition of CoQ synthesis, cancer, liver damage

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14
Q

pKa of glycine-conjugated bile acids?

A

4

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15
Q

pKa of taurine-conjugated bile acids?

A

2

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16
Q

What are the bile acids?

A

cholic and chenocolid

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17
Q

structure of cholic acid

A

alpha-hydroxy at 3, 7, 12

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18
Q

structure of chenocolic acid

A

alpha-OH at 3, 7

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19
Q

pKa of chenocolid/colic acids?

A

6

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20
Q

What modifications occur from cholesterol to bile acids?

A

1) 7-alpha-down OH, 2) oxidative cleavage of 3 C from side chain (COOH); 3) 3-alpha-down OH, 4) saturated 5-6, 5) maybe alpha-OH-down at C12

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21
Q

What are bacteria’s effects on bile acids?

A

deconjugate and dehyroxylate the 7-alpha-OH

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22
Q

What are the secondary bile acids?

A

deoxycholic acid (from cholic); lithocholic (from deoxycholic)

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23
Q

What does the body do to 2ndary bile acids?

A

reconjugate (do not re-hydroxylate)

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24
Q

Diagnosis of hypercholesteremia.

A

200+ mg/dL

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25
Q

How is hypercholesteremia caused?

A

1) familial (defective LDL receptor synthesis; hyperactive PCSK9); 2) high-cholesterol diet (down-regulates LDL receptor)

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26
Q

What contributes most to diabetic hypercholesteremia?

A

LDL receptor glycosylation

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27
Q

What proteins are in HDL?

A

1) apoCII, 2) apoE, 3) apo AI

28
Q

function of apoc2

A

stimulate LPL degradation of TGs

29
Q

function of apoE

A

ligand for liver receptor (CM remnants and HDL, not LDL)

30
Q

function of apoA1

A

stimulates LCAT to form CE

31
Q

function of CETP

A

HDL protein that exchanges CE for TG and PLs in VLDL

32
Q

proteins in nascent CM

A

apoB48

33
Q

what are the proteins in LDL?

A

apoB100; transfers apoC2 and apoE back to HDL

34
Q

What causes LDL oxidation?

A

superoxide radicals, NO, H2O2

35
Q

What substances are antioxidants?

A

vitamin C, E, carnitine, resveratrol, CoQ

36
Q

What is the depository form of cholesterol?

A

bile acids

37
Q

purpose of lipoproteins

A

transport FATS for storage and energy

38
Q

describe contents of VLDL

A

10% cholesterol; 15% CE; some phospholipids; mostly TG

39
Q

Describe location of cholesterol and CE in a lipoprotein.

A

cholesterol at membrane; CE at core

40
Q

What is LCAT and where is it located?

A

lecithin:cholesterol acyltransferase, blood

41
Q

What is ACAT and where is it located?

A

acyl:cholesterol acyltransferase, cells

42
Q

How is CE formed?

A

esterification of 3’OH

43
Q

What do statins look like?

A

mevalonate (competitive inhibitors)

44
Q

How many carbons in squalene?

A

30

45
Q

How many carbons in farnesyl Ppi?

A

15

46
Q

How many carbons in isopentenyl Ppi and demethylallyl Ppi?

A

5

47
Q

How many carbons in geranyl Ppi?

A

10

48
Q

What is HTGL?

A

hepatic TAG lipase

49
Q

What are the fates of LDL?

A

1) can enter LDL receptors on target cells; 2) can enter liver for cholesterol recycling; 3) can be oxidized

50
Q

Functions of HDL

A

1) exchanges lipids/proteins with CM and VLDL; 2) takes up cholesterol from cell surfaces and lipoproteins; 3) converts cholesterol to CE; 4) returns CE to liver by reverse cholesterol transport

51
Q

What proteins does the LDL receptor recognize?

A

apoE, apoB100

52
Q

How is cholesterol metabolism regulated?

A

1) primarily by HCR; 2) rate of LDL receptor synthesis; 3) rate of ACAT esterification

53
Q

Describe the specificity of the LPL receptor?

A

specific for blood lipoproteins relative to the other receptors

54
Q

What does cholesterol do after uptake?

A

1) increases membrane rigidity; 2) decreases HCR and LDLr synthesis; 3) stimulates ACAT for CE storage

55
Q

What does PCSK9 do?

A

binds to LDL receptor to initiate degradation

56
Q

When is the LDLr downregulated and how?

A

hi [cholesterol] and by PCSK9

57
Q

Describe the relative structure and specifity of LRP.

A

similar looking to LDL, but less specific for lipoproteins

58
Q

What proteins does LRP recognize?

A

alpha2-macroglobulin and TPA; apoE

59
Q

Where is LRP abundant?

A

liver, brian, placenta

60
Q

How is LRP regulated?

A

synthesis stimulated by insulin; otherwise unaffected by [cholesterol]

61
Q

Where are SR’s prevalent?

A

macrophages

62
Q

What things does the SR bind?

A

oxLDL; SRB1 binds cholesterol-loaded HDL

63
Q

What are fatty steaks?

A

foam cells formed by macrophage uptake of oxLDL, early sign of atherosclerosis

64
Q

How are SRs regulated?

A

not downregulated according to [cholesterol]

65
Q

Why does apoE not really contribute to hypercholesteremia in t2dm?

A

1) apoE inside HDL and for short timeframe; 2) LDL doesn’t use apoE

66
Q

How does an MI develop?

A

foam cells stimulate proliferation of smooth muscle; smooth muscle migrates to intimal layer; intimal cells release lipids and collagen/elastin to form fibrous cap; necrosis, calcification, hemorrhage, cap rupture leads to embolism

Drew 922 (12 decks)

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