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IMS > Cholesterol & lipoproteins > Flashcards

Cholesterol & lipoproteins Flashcards

1
Q

What are the functions of lipids

A
  • energy storage
  • cell memb. components
  • solubilise fat soluble vitamins
  • biosynthesis precursors
  • signalling molecules
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2
Q

Where is cholesterol obtained from

A
  • 25% diet

- synthesised in liver

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3
Q

How is cholesterol transplanted in blood

A
  • insoluble in blood plasma

- lipoprotein carriers

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4
Q
  • what are lipoproteins
A

Particles transporting lipids

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5
Q

What makes lipoproteins different

A

Protein:lipids

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6
Q

How are lipoproteins classified

A
  • density

- chemical

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7
Q

What are the different classes of lipoproteins and where are they made

A
  • chylomicrons (intestines)
  • VLDL (liver)
  • LDL (VLDL)
  • HDL (blood)
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8
Q

What is the function of chylomicrons

A
  • transport of dietary fats from intestines
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9
Q

What is the function of VLDL

A

Transport lipids to peripheral tissues

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10
Q

What is the function of LDL

A
  • main carrier of chol.

- provides cholesterol to peripheral tissues

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11
Q

What is the function of HDL

A
  • transport cholesterol to liver from peripheral tissues
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12
Q

What is the structure of lipoproteins

A
  • monolayer—> phospholipids, cholesterol and apolipoproteins
  • core—> cholesterol esters, triglycerides
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13
Q

What are apolipoproteins

A
  • protein strands

- surface of lipoproteins

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14
Q

What is the function of apolipoproteins

A
  • determine start + end points for cholesterol transport
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15
Q

What makes lipoproteins

A

Lipid + apolipoproteins

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16
Q

What are the 4 major classes of apolipoproteins

A
  • ApoA
  • ApoB
  • ApoC
  • ApoE
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17
Q

Where is ApoA found and what is its function

A
  • HDL
  • mediates efflux of cholesterol from peripheral cells
  • influx in liver
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18
Q

Where Ishtar function of ApoB

A
  • recognises ApoB/E receptors

- facilitates LDL uptake

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19
Q

What is the function of ApoC

A
  • activator of lipoprotein lipase
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20
Q

What is the function of ApoE

A
  • stabilise VLDL

- ligand for ApoB receptor

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21
Q

What is the synthesis of apolipoproteins in the small intestines regulated by

A
  • dietary fat intake
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22
Q

What is the apolipoproteins liver synthesis controlled by

A
  • drugs

- hormones

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23
Q

Give 2 examples of apolipoproteins function

A
  • regulate key enzymes in lipoproteins metabolism

- ligand for interaction with lipoprotein receptors

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24
Q

Give examples of apolipoproteins regulating key enzymes

A
  • ApoC-ii —> lipoprotein lipase

- ApoA-i lecithin-cholesterol acyltransferase

25
Q

Give examples of ligand interacting with lipoprotein receptors

A
  • apoB100 & ApoE in LDL receptors

- ApoA-i for HDL receptors

26
Q

what is the structure of LDL

A
  • phospholipids & free colesterol on SM
  • hydrophobic core –> triglyceride & cholestryl esters
  • ApoB
27
Q

what is the structure of HDL

A
  • SM (same as LDL)
  • core (same as LDL)
  • Apo A-I
  • Apo A-ii
28
Q

what is the function of ApoA-i and Apo-Aii in HDL

A
  • protect against oxidation

- anti-inflammatory

29
Q

where are chylomicrons made & what do they do

A
  • intestine

- transport triglycerides & cholesterol in blood

30
Q

what are triclycerides hydrolysed by and what are they used for

A
  • lipoprotein lipase –> fatty acids

- energy source/store

31
Q

what happens to chylomicrons after hydrolysis of triglycerides

A
  • shrink

- back to liver

32
Q

where are VLDL made? what do they do? why does lipoprotein lipase act on them

A
  • liver
  • transport lipids to tissue
  • release fatty acids for tissues
33
Q

what happens to LDL from VLDL

A
  • taken up by target cells
  • by LDL receptors
  • digested in lyssome
  • release cholesterol
34
Q

what is the function of HDL? where are they synthesised?

A
  • remoce cholesterol

- blood

35
Q

what are lipoprotein receptors

A

membrane-bound receptors

36
Q

what is the function of lipoprotein receptors

A
  • enable enterance of cholesterol to cells
37
Q

what does LDL receptor bind to

A
  • apoB-100

- apoE

38
Q

what is LDL receptor gene expression regulated by

A
  • intracellular cholesterol concentration
39
Q

what do high levels of intracellular cholesterol result into

A
  • supress LDL receptor synthesis
  • chol not taken up by cells, remain in blood
  • deleterious onsequences
40
Q

how does HDL protect aganst arthesclorisis

A
  • scavenges cholesterol back to liver, excerted by bile

- reverse Cholesterol Transport

41
Q

what is dyslipidaemias

A
  • familial hypercholesterolaemia
  • mutation in LDL receptor
  • cells can’t take up LDL
42
Q

what does dyslipidaemias result in

A
  • blood LDL increases
  • excess cholesterol in arteries
  • higher risk of atherosclerosis
43
Q

what is cholesterol essential component of

A
  • cell membranes
  • bile acids
  • steroid hormones
  • fat-soluble vitamins
44
Q

what do high serum levels indicate

A
  • risk of cardiovascular disease
45
Q

what are the cardiac clincal manifestations of artherosclerosis

A
  • chest pain
  • palpitations
  • heart attck
46
Q

what are the cerebral clinical implications of atheroscllerosis

A
  • stroke

- cerebral haemorrhage

47
Q

what are the peripheral clinical implications of athersclerosis

A
  • pain
  • ischaemia
  • ulceration
  • gangrene
48
Q

what are the stages of development of athresclerosis plaque

A
  • fatty streak
  • fibrous plaque
  • advanced plaque
49
Q

what is the cholesterol-synthetic pathway

A
  • HMG-CoA –> Mevalonate –> IPP –> FPP –> squelene –> cholesterol
50
Q

what is the enzyme converting HMG-CoA to mevalonate

A

HMG-CoA

51
Q

how do statins reduce the risk of hypercholestrolaemia

A
  • prevent cholesterol synthesis in liver

- act as HMG-CoA reductase inhibitors –> no mevalonate

52
Q

what are pleitropic effects

A
  • unanticipated

- undesirable

53
Q

what are FPP & GGPP

A

isoprenoids

54
Q

how are Ras & Rho prenylated

A
  • Ras: Farnesylated (FPP)

- Rho: Geranylgeranylated (GGPP)

55
Q

what are statins’ pleitropic effects

A
  • improve endothelial dysfunction
  • antioxidant
  • inhibit iflammatory response
  • stabilise artherosclerotic plaques
56
Q

what are PCSK9 expressed by

A
  • liver

- intestine

57
Q

what is the role of PCSK9

A
  • lipid metabolism
  • promote intracellular degenaration of LDL-R
  • prevents recycling of LDL-R to cell surface
  • reduces LDL-R population
58
Q

what does PCSK9 inhibition do

A

increase LDL uptake

IMS (18 decks)

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