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Case 4 > Lipids and Cardiovascular Disease > Flashcards

Lipids and Cardiovascular Disease Flashcards

1
Q

What are lipids chemically characterised by

A

Hydrophobic properties

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2
Q

Which lipids are relevant to CVD

A

Cholesterol, fatty acids, triacylglycerol (triacylceride) and phospholipids

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3
Q

What do and don’t lipids dissolve in

A

Dissolve in organic solvents (alcohols) but not aqueous solvents

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4
Q

What is cholesterol

A

An alcohol, multi-ring structure (free cholesterol) which possesses ester fatty links to fatty acids in the body

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5
Q

What does the fact that cholesterol in the body is amphiphilic and hydrophobic mean

A

It is completely insoluble

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6
Q

What do fatty acids differ in

A

Chain lengths and types of bonds

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7
Q

Describe liquid fatty acids

A

More polyunsaturated (more double bonds) meaning that they are less linear.

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8
Q

Describe solid fatty acids

A

They are saturated

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9
Q

Which fatty acids are essential

A

Eicosanoids which contain prostaglandins, thomboxanes and leukotriens. Alpha-linolenic acid (omega-3) and linoleic acid (omega-6) are essential fatty acids

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10
Q

What are trans fatty acids

A

Hydrogenated fats

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11
Q

How are trans fats produced

A

Synthetically by hydrogenation changes. The conformation change from cis to trans fatty acids seems to be harmful

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12
Q

What do trans fats do in the body

A

Raise levels of LDL and lower levels of HDL, therefore the use of trans fats is being reduced

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13
Q

What features do phosopholipids have in common with triglycerides

A

They have a glycerol backbone and two fatty acids (non-polar) but also have a phosphate group (polar)

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14
Q

What does polarity determine

A

How fats are distributed within circulation

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15
Q

How are fats transported

A

As lipoproteins

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16
Q

Describe the structure of lipoproteins

A

Shell and core. Inside the core there are hydrophobic lipids (cholesterol ester and triglyceride), inside the shell there are lipids with a polar component (phospholipids have phosphate group to outside, cholesterol have alcohol group to outside) which forms the shell on the outside which interacts with the plasma

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17
Q

Describe the protein component of lipoproteins

A

Protein component which are specialised proteins which are imbedded in the membrane and have a polar exterioir and non-polar interioir

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18
Q

How many major lipoproteins are there

A

5

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19
Q

How are the different lipoproteins defined

A

By their density, they precipitate to different extents depending on their composition

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20
Q

What are the most dense lipoproteins

A

HDL (high density lipoproteins)

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21
Q

What are the least dense lipoproteins

A

Chylomicrons

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22
Q

What is the major difference between HDL and chylomicrons

A

Chylomicrons are triglyceride and HDL are protein. Protein makes HDL dense and triglycerides make chylomicrons buoyant

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23
Q

Describe the proteins in HDL

A

Apo A1 receptor ligand

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24
Q

Describe the proteins in chylomicrons

A

Apo B48 receptor ligand (produced by splicing of messenger RNA)

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25
Q

Describe the proteins in LDL

A

Apo B100 receptor ligand

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26
Q

Describe the proteins in VLDL

A

ApoCII cofactor lipoprotein lipase

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27
Q

Describe the proteins in IDL

A

ApoE receptor ligand

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28
Q

What is the function of chylomicrons

A

Transport triglycerides from the digestive system in the gut to the liver

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29
Q

How are chylomicrons absorbed into the liver

A

Through lacteals

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30
Q

What does the liver do with the triglycerides in chylomicrons

A

Makes VLDL

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31
Q

What is the function of VLDL

A

Transports triglyceride from the liver to the tissue

32
Q

What is IDL

A

A remnant from chylomicrons

33
Q

What is VLD

A

An intermediate between chylomicrons and LDL

34
Q

What is the function of LDL

A

Transports cholesterol from the liver to tissues

35
Q

What is the function of HDL

A

Transports cholesterol from the tissues back to the liver (reverse cholesterol transport)

36
Q

What are the 3 main lipid pathways

A

Exogenous pathway, endogenous pathway and reverse cholesterol pathway

37
Q

Describe the exogenous pathway

A

Chylomicrons are produced from triglycerides in the gut and the circulate through capillaries once absorbed into the circulation. Triglyceride is taken up by enzyme lipoprotein lipase and bind to free fatty acid which becomes adipose tissue. Triglycerides are lost leaving chylomicron remnants which is taken back up into the liver and is recycled

38
Q

Describe the endogenous pathway

A

Occurs internally from the liver. The liver synthesises VLDL which is a triglyceride rich lipoprotein. Triglyceride then leaves the circulation by the action of the enzyme lipoprotein lipase. VLDL then becomes IDL. IDL then is converted to LDL after being taken up in the liver via the enzyme hepatic lipase. The LDL then transports cholesterol to tissue, particularly muscle and other tissues that require cholesterol

39
Q

Describe the reverse cholesterol pathway

A

Empty HDL picks up cholesterol from tissues, particularly muscle, and transports it back to the liver in a process called reverse cholesterol transport pathway

40
Q

What are lipids a risk factor for

A

Atherosclerosis

41
Q

What cores do atherosclerotic plaques have

A

Lipid cores

42
Q

What is the evidence for lipids and CVD

A

Pathology, epidemiology, inborn errors, effects of treatment

43
Q

Describe the formation and course of plaques

A

The process of atherosclerosis takes years. To begin with there is endothelial damage then a fatty streak forms then a plaque forms with a lipid core. Plaques tend to rupture as they are large and have a lipid core

44
Q

Describe a grade I plaque

A

Foam cells

45
Q

Describe a grade II plaque

A

Fatty streak

46
Q

Describe a grade III plaque

A

Extracellular fatty streak

47
Q

Describe a grade IV plaque

A

Lipid core

48
Q

Describe a grade V plaque

A

Atherosclerotic plaque lipid core embedded in fibrosis

49
Q

Describe a grade VI plaque

A

Complicated atherosclerotic plaque (plaque rupture, thrombosis, haemorrhage)

50
Q

What does HDL appear to be

A

Protective against CHD or is a marker of something else which is protective

51
Q

What is familial hypercholesterolaemia

A

An inborn error which affects LDL receptors

52
Q

What happens if you have no LDL receptors (FH homozygotic)

A

You develop heart disease as a child

53
Q

What happens if you have one copy the LDL receptor gene (FH heterozygotic)

A

You have half the number of receptors meaning that you have a significant risk of developing CVD

54
Q

What is FH a model disorder for

A

Cell surface receptors, receptor mediated endocytosis and atherosclerosis

55
Q

What is an LDL receptor

A

A transmembrane protein with an LDL binding component

56
Q

Describe the action of LDL receptors

A

APOB of the LDL binds to the receptor which results in LDL being removed from the blood. LDL is broken down which releases cholesterol carried by LDL

57
Q

What is cholesterol released from LDL converted to

A

Bile, then excreted

58
Q

What does the LDL receptor recycle

A

PCSK9

59
Q

Describe the dominancy of FH

A

It is autosomal dominant

60
Q

When does FH occur

A

When there is a mutation in the LDL receptor pathway

61
Q

When does CHD usually develop in those with FH

A

Around 20 years early

62
Q

What treatment is effective in reducing CVD

A

Statins

63
Q

What are the clinical signs of FH

A

Corneal arcus, xanthelasma, tendon xanthoma. The clinical signgs of FH are due to hypercholesterolemia

64
Q

Why do we treat hyperlipidaemia

A

To reduce CHD rates

65
Q

What are effective in reducing high cholesterol

A

Statins

66
Q

How do statins work

A

They limit the activity of HMG-CoA reductase and therefore inhibit cholesterol synthesis. The decrease in cholesterol means that cells upregulate cholesterol receptors and therefore remove cholesterol from circulation

67
Q

Via what mechanism do statins act

A

Competitive inhibition

68
Q

What are the 4 different statins available in the UK

A

Atorvastatin, simvastatin, pravastatin and rosuvastatin

69
Q

What statin is used in children

A

Pravastatin

70
Q

Which statin is the most intensive and expensive

A

Rosuvastatin

71
Q

What is a possible side effect of statins

A

Myositis (inflammation and degeneration of muscle tissue)

72
Q

Who needs to take statins

A

Anyone whose risk is more than 10% for the next 10 years

73
Q

What are other lipid lower drugs

A

Fibrates, bile acid sequestrants, cholesterol uptake inhibitors, cholesterol ester transfer protein inhibitors (all more specialist)

74
Q

Who gets the highest benefit from statins

A

Patients who have already had a heart attack and are using statins as a secondary prevention

75
Q

What do statins do to plaques

A

Stabilise plaques and prevent them from rupturing

Case 4 (7 decks)

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