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The Cardiovascular System > Lipids and Cardiovascualr Disease > Flashcards

Lipids and Cardiovascualr Disease Flashcards

1
Q

What are lipids

A

Organic compounds which are poorly soluble in water but soluble in organic solvents.

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2
Q

What are the 5 categories of lipids

A

Steroids, fat-soluble lipids, phospholipids, sphingolipids and triglycerides.

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3
Q

What is the important lipid in cardiovascular disease

A

Cholesterol (which is a steroid precursor) and phospholipids

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4
Q

By what molecule is cholesterol carried around the body

A

Lipoproteins

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5
Q

What is ApoB

A

The protein component of lipoprotiens

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6
Q

How are cholesterol and triglycerides transported around the body

A

Via the circulation

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7
Q

What are the 5 types of lipoprotien

A

Chylomicrons, very low density lipoprotein (VLDL), low density lipoprotein (LDL), intermediate density lipoprotein (IDL) and high density lipoprotein (HDL)

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8
Q

What’s the biggest lipoprotein

A

Chylomicrons

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9
Q

In what organ are dietary lipids created

A

The small intestine

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10
Q

In what organ are endogenous lipids created

A

The liver

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11
Q

How do lipids get from the peripheral tissues back to the liver for hepatic excretion.

A

Reverse cholesterol transport.

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12
Q

What are the three main pathways for transport and metabolism of cholesterol

A

Endogenous, exogenous and reverse cholesterol transport.

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13
Q

What type of cholesterol is the exogenous pathway concerned with

A

Dietary cholesterol

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14
Q

What type of cholesterol is the endogenous pathway concerned with

A

Cholesterol made by the body in the liver

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15
Q

What is the role of the reverse cholesterol transport pathway

A

To carry cholesterol from the peripheral tissues back to the liver.

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16
Q

How does the exogenous pathway work

A

The exogenous lipids are broken down. Triglyceride is absorbed into the small intestine and LPL (lipoprotein lipase) is activated which breaks down triglycerides to produce glycerol and fatty acids. These are taken up by muscle and adipose tissue. The remnants are chylomicrons which are taken up by the liver.

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17
Q

What is the important enzyme in the exogenous pathway

A

Lipoprotein lipase (LPL)

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18
Q

What is the role of LPL

A

To break down chlyomicrons into triglyceride and fatty acids.

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19
Q

What happens in the endogenous pathway

A

VLDL is made. VLDL is attacked by LPL to release glycerol and fatty acids to be taken up by muscle and adipose tissue. As this happens VLDL is converted to IDL and then LDL.

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20
Q

In what form can cells use and metabolise cholesterol

A

LDL as most cells have LDL receptors

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21
Q

What should happen to excess cholesterol

A

It should be returned to the liver.

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22
Q

What is the role of HDL

A

To return cholesterol to the liver

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23
Q

What happens to the cholesterol when it is returned to the liver by HDL

A

It is stored or gotten rid of,

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24
Q

What does cholesterylester transfer protein (CETP) do

A

It disrupts the return of cholesterol back to the liver by HDL be transferring HDL to VLDL so that the endogenous pathway is carried out

25
Q

What is the name of the enzyme which converts HDL to VLDL disrupting the reverse cholesterol transport pathway

A

The cholesterylester transfer protein (CETP)

26
Q

What allows cholesterol to be carried in HDL

A

ABC-A1 transporter

27
Q

What do apolipoproteins do

A

Determine the behaviour of lipoproteins

28
Q

What type of apolipoprotein is present in chylomicrons

A

ApoB48

29
Q

What type of apolipoprotein is present in IDL

A

ApoB100

30
Q

What type of apolipoprotein is present in HDL

A

ApoA1

31
Q

What type of cholesterol causes atherosclerosis

A

Non-HDL cholesterol

32
Q

What is the effect of raised HDL cholesterol on rates of atherosclerosis

A

Raised HDL decreases the rate of atherosclerosis

33
Q

What drugs are used in cardiovascular disease to reduce cholesterol

A

Statins

34
Q

What leads to the formation of fatty streaks

A

Damage to the arterial wall and high concentrations of LDL.

35
Q

What happens to LDL molecules before they become incorporated into foam cells

A

They are oxidised by oxygen free radicals

36
Q

What is a fatty streak

A

The collection of foam cells in the arterial wall.

37
Q

How does an atheromatous plaque form from a fatty streak

A

Smooth muscle cells from the medial layer of the blood vessel migrate into the intimal layer. Some foam cells undergo necrosis or apoptosis to leave extracellular cholesterol and a fibrous cap forms.

38
Q

what happens if the lesion is more fibrous and contains less cholesterol

A

It is less likely to rupture and leads to reduced blood flow which creates stable angina if in the coronary arteries.

39
Q

What is an inherited disorder of lipoprotein metabolism

A

Familial hypercholesterolaemia

40
Q

What causes familial hypercholesterolaemia

A

A mutation in the LDL receptor which means LDL cannot be up-taken efficiently by cells in peripheral tissues so hangs around in the circulation

41
Q

What happens to LDL that cannot be taken up by cells in familial hypercholesterolaemia

A

It is taken up by ,macrophages to create foam cells which enter the endothelium of blood vessel walls to create fatty streaks and eventually an atherosclerotic plaque.

42
Q

What does familial hypercholesterolaemia lead to if left untreated

A

Premature CHD onset.

43
Q

What is one of the tell-tale signs of familial hypercholesterolaemia

A

Stigmata of hyperlipodaemia

44
Q

What is stigmata of hyperlipodaemia

A

Cholesterol tends to gather on tends and around the eyes and this can clearly be seen in patients when they present.

45
Q

What can routine laboratory measurements tell you about lipids

A

The total cholesterol, HDL cholesterol and triglycerides. LDL cholesterol has to be calculated, it is not measured.

46
Q

What drugs are used to treat CVD

A

ACE-inhibitors, beta-blockers, aspirin, statins.

47
Q

What are the roles of ACE-inhibitors and beta-blockers

A

To reduce post-MI mortality by reducing blood pressure.

48
Q

What are the roles of aspirin and statins

A

To reduce CVD recurrence and mortality

49
Q

What is recommended for primary prevention of CVD

A

Lifestyle changes including -

  • reduce fat, carbohydrates and salt in the diet
  • carry out aerobic exercise
  • BMI between 20 and 25kg/m2
  • reduce alcohol consumption
  • quit smoking
50
Q

How do you decide who to treat

A

Use the risk calculator as there are many factors which contribute to CVD. This gives % risk for CVD event in the next 10 years. In Scotland - treat those with 20% risk or more. In England - treat those with 10% risk or more (differing guidelines)

51
Q

Which socioeconomic class are most affected by CVD

A

The least affluent.

52
Q

What are three examples of lipid-lowering drugs

A

Statins, ezetimibe, fibrates

53
Q

What is the mechanism of action of statins

A

They reduce LDL cholesterol by inhibiting the rate limiting step of cholesterol synthesis. Liver cells become deplete of LDL, making them want to uptake more LDL.

54
Q

What is the mechanism of action of ezetimibe

A

It inhibits cholesterol absorption at the small intestine.

55
Q

What is the mechanism of action of fibrates

A

Cause an increase in LPL activity leading to enhanced IDL and LDL uptake and reduced VLDL synthesis.

56
Q

What is the name of the new lipid-lowering drugs

A

PCSK9-inhibitors

57
Q

What is the mechanism of action of PCSK9-inhibitors

A

PCSK9 is crucial in cholesterol metabolism. it targets LDL receptors for destruction by lysosomes. If you inhibit this action, more LDL will be taken up by cells

58
Q

What are the names of 2 PCSK9 inhibitors

A

Alirocumab and evolocumab

The Cardiovascular System (15 decks)

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