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Cardiovascular > Lipid Metabolism And Cardiovascular Disease > Flashcards

Lipid Metabolism And Cardiovascular Disease Flashcards

1
Q

Solubility of Lipids

A

Insoluble/ slightly soluble in water

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2
Q

What are lipids essential for?

A

Membrane biogenesis and integrity

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3
Q

Example of Non—polar lipids

A

Triglycerides

Cholesterol esters

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4
Q

How are non-polar lipids transported?

A

In blood by lipoproteins

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5
Q

HDL and LDL levels associated with atherosclerosis

A

Increased LDL or particles rich in triacylglycerols; TAGs

Decreased HDL

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6
Q

Causes of CVD

A

Poor diet and exercise

Genetic factors eg familial hypercholesterolaemia

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7
Q

What comprises lipoproteins

A

Hydrophobic core

Hydrophilic coat

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8
Q

What comprises the hydrophobic core?

A

Esterified cholesterol

Triacylglycerols

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9
Q

What comprises the hydrophilic coat?

A

Monolayer of amphipathic cholesterol, phospholipids at at least one apoproteins

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10
Q

What allows lipoproteins to bind to cells?

A

Apoproteins recognised by receptors in liver

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11
Q

4 classes of lipoproteins

A

HDL
LDL
VLDL
Chylomicrons

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12
Q

What differentiates the classes of lipoproteins?

A

Size

Proportions of apoproteins

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13
Q

Which apoproteins does HDL contain?

A

ApoA-I

ApoA-II

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14
Q

Which apoproteins does LDL contain?

A

ApoB-100

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15
Q

Which apoproteins does VLDL contain?

A

ApoB-100

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16
Q

Which apoproteins do chylomicrons contain?

A

ApoB-48

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17
Q

Role of ApoB-containing lipoproteins

A

Transport TAGs to muscle cells for biogenesis and adipocytes for storage

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18
Q

Where are chylomicrons formed?

A

Intestinal cells

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19
Q

What pathway do chylomicrons follow when transporting dietary triglycerides?

A

Exogenous

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20
Q

Where are VLDL formed?

A

Liver cells

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21
Q

What pathway do VLDLs follow when transporting TAGs made in liver?

A

Endogenous

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22
Q

Life cycle of ApoB-containing liposomes

A

Assembly of ApoB-100 + 48
Intravascular metabolism- involves hydrolysis of TAG core
Receptor mediated clearance

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23
Q

Assembly of chylomicrons

A

Monoglyceride and free fatty acid synthesise TAG in enterocyte
Cholesterol is esterified in the enterocyte also
These then join, along with apoB-48 in the ER to form a chylomicron
The joining is facilitated by microsomaltriglyceride transfer protein

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24
Q

Assembly of VLDL particles

A

Assembled in liver hepatocytes from free fatty acids

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25
Q

How are Chylomicrons and VLDL particles activated?

A

Transfer of apoC-II from HDL

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26
Q

Lipoprotein Lipase

A

Lipolytic enzyme associated with endothelium of capillaries in adipose and muscle tissue

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27
Q

Which apoprotein facilitates binding of chylomicrons and VLDLs to LPL?

A

ApoC-II

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28
Q

Why does LPL hydrolyse core TAGs?

A

Free fatty acids and glycerol, which enter tissues

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29
Q

Chylomicron and VLDL remnants

A

Particles depleted of triglycerides but still contain cholesterol esters

30
Q

What is the clearance of LDL particles dependent on?

A

LDL receptor (ApoB/E receptor) expressed by liver (and other tissues, but liver is most important)

31
Q

How does cellular uptake of LDL particles occur?

A

Via receptor mediated endocytosis

32
Q

Where is cholesterol released by cholesterol esters and by which process?

A

Within the cell at the lysosome

Hydrolysis

33
Q

What does released cholesterol do?

A

Inhibit HMG-CoA reductase
Regulates LDL receptor expression
Stored as CE or used as precursor for bile salt synthesis

34
Q

What does LPL cause chylomicrons and VLDL particles to do?

A

Become enriched in CE due to TAG metabolism, they then dissociate from LPL

35
Q

What happens after Chylomicrons and VLDL dissociate from LPL?

A

ApoC-II is transferred back to HDL particles in exchange for ApoE
- particles are now remnants

36
Q

Where do remnants from HDL go?

A

Return to liver, where they are further metabolised by hepatic lipase

37
Q

What clears all chylomicron and half of VLDL remnants?

A

Receptor mediated endocytosis into hepatocytes

38
Q

What happens to remaining VLDL remnants?

A

They lose more TAG via hepatic lipase and become smaller and enriched in CE via IDL

39
Q

What do LDLs from IDLs lack and retain?

A

They lack apoE

They retain apoB-100

40
Q

What is apoE?

A

A high affinity ligand for receptor mediated clearance

41
Q

What is the ‘bad’ cholesterol?

A

LDL

42
Q

Why is LDL ‘bad’?

A

It is oxidised in intima of artery and uptaken by macrophages convert them to cholesterol-laden foam cells
These form a fatty streak
An Atheromatous plaque forms from lipid core (dead foam cells ) and fibrous cap (SM and CT)

43
Q

Role of HDL

A

Removing xs cholesterol from cells by transporting it to liver in plasma

44
Q

Why must cholesterol be transported to the liver?

A

It is the only organ which can eliminate cholesterol

- it is either secreted into bile or used to make bile salts

45
Q

Pre-Beta-DL

A

Unesterified cholesterol, small amount of surface phospholipid and apoA-I

46
Q

Where does pre-beta-HDL mature and what does it become?

A

In the plasma

Spherical alpha HDL

47
Q

Reverse cholesterol transport

A

Mature HDL accepts xs cholesterol from plasma membrane of cells and delivers it to liver

48
Q

Role of scavenger receptor-B1

A

Allows HDL to transfer cholesterol and cholesteryl esters into hepatocytes

49
Q

Which protein mediates transfer of cholesteryl esters from HDL to VLDL and LDL?

A

Cholesterol ester transfer protein

50
Q

Lipid lowering drugs

A

Statins and fibrates

51
Q

Why are statins the drug of choice when reducing LDL?

A

Reduces LDL cholesterol by up to 60%
Decreases TGAs by up to 40%
Increases HDL by approx 10%

52
Q

Examples of Statings

A

Simvastatin

Atorvastatin

53
Q

Which enzyme do stains competively inhibit?

A

3-hydroxy-3-methylglutaryl coA reductase

* this is the rate limiting step in cholesterol synthesis in hepatocytes

54
Q

How does decreasing hepatocytes cholesterol synthesis reduce LDL levels?

A

It causes a compensatory increase in LDL receptor expression and therefore enhances LDL clearance

55
Q

In what circumstance are LDLs ineffective? Why?

A

Homozygous familial hypercholesterolaemia

There are no LDL receptors

56
Q

Benefits of statins

A

Decreased inflammation
Reversal of endothelial dysfunction
Decreased thrombosis
Stabilisation of atherosclerotic plaques

57
Q

Adverse effects of statins

A 
Myositis 
Rhabdomyolosis (risk higher if combined with fibrate)
58
Q

Effect of Fibrates

A

Up to 50% decrease in TGAs
Up to 15% decrease in LDL
Up to 20% increase in HDL

59
Q

Examples of Fibrate

A

Bezafibrate

Gemfibrozil

60
Q

What is the first line drug used for patients with very high TGA levels?

A

Fibrates

61
Q

How do fibrates enhance the transcription of several genes?

A

They act as agonists of PPAR-alpha (nuclear recptor)

62
Q

Adverse effects of fibrates

A

Myositis
Avoid combo with statins
Avoid alcoholics predisposed to hypertriglyceridaemias

63
Q

Drugs that inhibit cholesterol absorption

A

Bile acid binding resins eg colestyramine, colestipol, colsevelam

64
Q

How do bile acid binding resins inhibit cholesterol absorption?

A

They cause excretion of bile salts, meaning more cholesterol can be converted to by salts by interrupting enterohepatic recycling

65
Q

Effect of bile salts on TGAs and LDLs

A

Decreases TGA absorption

Increases LDL receptor expression

66
Q

Adverse effect of bile acid binding resins

A

GI tract irritation

67
Q

How does Ezetimibe work?

A

It inhibits NPC1L1 TP in enterocytes, reducing cholesterol absorption’s

68
Q

Effect of ezetimibe on LDL

A

Decrease of about 18% in LDL levels; little change in HDL

69
Q

What must ezetimibe be used in combination with when it doesn’t achieve a sufficient response alone?

A

Statins

70
Q

Adverse effects of ezetimibe

A

Diarrhoea
Abdominal pain
Headaches
Not to be used in breast feeding females

Cardiovascular (14 decks)

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