LMP301 Lecture 6: Lipids & Cardiac Disease Flashcards

0
Q

IHD

A

Ischemic heart disease

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1
Q

Ischemic heart disease

A

Inadequate supply of blood to the heart; some kind of blockage causes heart to stop working.

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2
Q

____ of deaths from IHD can be prevented

A

> 1/2

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3
Q

Differences between men and women in terms of IHD

A

Symptoms in women are less characteristic than men -> under diagnosis
Risk for men and women are the same

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4
Q

Disease that may result from fat deposits in the arteries

A
  1. IHD
  2. Cerebrovascular disease
  3. Peripheral vascular disease
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5
Q

Cerebrovascular disease

A

Stroke

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6
Q

Peripheral vascular disease

A

Blood can’t flow the the extremeties

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7
Q

Where is the lipid core found?

A

Nested in the intima

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8
Q

What holds the lipid core in place?

A

Fibrous cap

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9
Q

4 types of lipids

A
  1. Cholesterol
  2. Triglycerides
  3. Phospholipids
  4. FA
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10
Q

Which lipids are used for fule?

A

TG and FA

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11
Q

Which lipids can be found in the membrane?

A

Cholesterol & phospholipids

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12
Q

Functions of cholesterol

A

Production of hormones

Membrane structure

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13
Q

Functions of phospholipids

A

Make up cell membranes

Signalling

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14
Q

Transporter for lipids

A

Lipoproteins carry circulating lipids in plasma & lympth

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15
Q

Carriers for FFA

A

Albumin

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16
Q

Exogenous pathway for lipids

A

Lipids consumed from fats

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17
Q

Endogenous pathway for lipids

A

Lipids made by the body

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18
Q

Outline exogenous pathway for lipid metabolism

A

Dietary fats transported in body by chylomicrons (used in muscle or stored in adipose). Remnant returns to liver to be metabolized. Liver secretes bile which help emulsify fats in the intestines.

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19
Q

Outine endogenous pathway of lipid metabolism

A

Liver produces VLDL -> broken down into TG and IDL. TG goes to muscles and adipose tissue while IDL can return to liver or become LDL. LDL deposits cholesterol in extra-hepatic cells, then return to liver.

Liver can also make HDL which picks up extra cholesterol from cells-> return to liver to be metabolized.

Liver produce bile from the cholesterol which is used in the exogenous pathway

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20
Q

Extra-hepatic cells

A

Cells other than liver cells

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21
Q

What does HDL do?

A

Reverse cholesterol transport

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22
Q

Reverse cholesterol transport

A

Take extra cholesterol from cells and returns to liver (prevent buildup)

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23
Q

List the lipoproteins in order of least dense -> most

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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24
Q

Which is the largest lipoprotein?

A

CM

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25
Q

Purpose of CM

A

Transport TG and TC

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26
Q

What happens to the CM remnant?

A

Metabolized by the liver to give VLDL

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27
Q

Purpose of VLDL

A

Carry mostly TG and some TC to adipose & muscle tissues

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28
Q

What happens to VLDL during transfer?

A

Some of it’s surface components are lost

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29
Q

VLDL ->

A

IDL

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30
Q

Purpose of IDL

A
  1. Return to liver

2. Become LDL

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31
Q

Purpose of LDL

A

Carries TC to peripheral tissues

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32
Q

What do LDL bind to?

A

Specialized receptors on liver & peripheral cells

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33
Q

Atherogenic

A

Promote formation of fatty plaques in the arteries

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34
Q

Which LP is atherogenic?

A

LDL

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35
Q

Statins try to lower…

A

LDL

36
Q

HDL is composed of

A

proteins & phospholipids

37
Q

Where is HDL made?

A

Liver

38
Q

What happens to HDL during transport?

A

Accepts TC from other lipoproteins; increase in size (HDL-1 -> HDL-2 -> HDL-3)

39
Q

Purpose of HDL

A

Carries TC from peripheral tissues to liver (for removal) using reverse cholesterol transport

40
Q

What is the only organ that can excrete significant amounts of cholesterol?

A

Liver

41
Q

How does the liver excrete cholesterol?

A

Bile salts

42
Q

Importance of bile salts?

A

Absorbs fat-soluble vitamins in the intestine

43
Q

2 types of lipid disease

A
  1. Inherited (genetic factors)

2. Acquired (risk factors)

44
Q

Familial hypercholesterolemia

A

High levels of cholesterol

45
Q

FHC

A

Familial hypercholesterolemia

46
Q

Familial hypertriglyceridemia

A

Genetic mutations that cause high levels of triglycerides

47
Q

2 types of inherited lipid disease

A
  1. FHC
  2. Familial hypertriglyceridemia

Combination of 1 and 2.

48
Q

Causes of FHC

A

Defect in LDL receptor: LDL is unable to return to liver, so excess amount circulates in the blood

49
Q

Risk for those w/ heterozygous FHC gene

A

have MI in their 30’s

1:500 people

50
Q

Risk for those homozygous for FHC gene

A

have MI in childhood (1:1000000)

51
Q

Marker for FHC

A

Xanthoma

52
Q

Xanthoma

A

Build-up of fatty deposits in soft tissues (e.g. eyelids)

53
Q

Thrombosis

A

When the fibrous cap breaks and ruptures the artery, blood clot that forms at the site of damage will clog the artery

54
Q

How to treat MI and stroke surgically?

A

Busters:

  1. Enzymes that break the clot
  2. Balloons to open up the vessel
55
Q

Pathogenesis of IHD

A
  1. Oxidant status
  2. Inflammatory response markers
  3. Lipoprotein(a)
56
Q

Oxidant status

A

LDL in lipid plaque become oxidized by free radicals.

57
Q

Marker for oxidant status

A

Homocysteine in some patients (reducing AA)

58
Q

Inflammatory response markers

A

Tissue damage at atheroma triggers inflammatory response.

Oxidation of LDL also triggers inflammatory response

59
Q

Marker for inflammatory response?

A

CRP

60
Q

CRP

A

C-reactive protein

61
Q

C-reactive protein

A

Acute phase reactant (appears quickly) when body has an inflammation.
Used to identify those at higher risk for IHD.

62
Q

Role of Lp(a) in IHD

A

Interfere with plasminogen process.

Plasminogen is anti-clotting factor, so Lp(a) causes clotting to happen.

63
Q

How to prevent IHD?

A
  1. Routine screening of cholesterol after the age of 40

2. If screen shows problems: fasting lipid profile

64
Q

TC =

A

LDL + HDL + VLDL

65
Q

VLDL =

A

TG / 2.2 (MUST BE FASTING)

66
Q

LDL =

A

TC - (HDL + TC/2.2)

67
Q

Which lipoprotein is usually calculated? What conditions must be met?

A

LDL-C

TG must be less than 4.5 mmol/L

68
Q

Lipid indicators of risk for IHD

A
  1. TC : HDL ratio
  2. Apo-B
  3. Apo-A1
69
Q

Apo-B is a marker for…

A
VLDL
IDL
LDL
Lp(a)
(1:1 ratio)
70
Q

Apo-B might be more useful in patients with…

A

metabolic syndrome

71
Q

Apo-A1 is a marker for…

A

HDL

1:1 ratio

72
Q

Benefit of measuring Apo-B and A1 over lipid profile

A

NO need to fast

73
Q

Problems with cholesterol screening

A
  1. Cholesterol in IHD patients and non-IHD patients may be the same
  2. HDL is not accounted for
  3. Variability in cholesterol measurement (up to 12%)
  4. Other risk factors
  5. Low cholesterol diets hard to follow
  6. Research for cholesterol <-> IHD outdated
  7. Cost high
74
Q

Framingham heart study

A

Model for 10-year risk of coronary artery disease (guildline for heart disease risk factors).
ATP-III is the treatment guidelines developed.

75
Q

What automatically puts you at high risk for IHD?

A

Diabetes II

76
Q

Risk factors associated with IHD from the Framingham heart study

A
  1. Age
  2. HDL
  3. TC
  4. BP
  5. Smoker
  6. Diabetes
  7. Sex
77
Q

10-year risk score

A

Points that = some level of risk for developing CVD in the next 10 years

78
Q

Risk categories from the 10-year risk score

A

High, moderate, low

79
Q

Metabolic syndrome (X)

A

A cluster of risk factors that are associated with heart disease & diabetes.

Getting 3 or more of those factors = metabolic syndrome

80
Q

Key metabolic changes (metabolic syndrome)

A
  1. Impaired fasting glucose (Insulin-resistance)

2. Abdominal fat (small-dense LDL)

81
Q

management of IHD

A
  1. TLC: therapeutic lifestyle changes
  2. Drugs
  3. CABG: coronary artery bypass graft
82
Q

2 TLC changes to manage IHD

A
  1. Exercise

2. Vegetarian diet

83
Q

CABG

A

Vein grafted: replace coronary artery

84
Q

AMI

A

Acute Myocardial infarction

85
Q

Symptom for AMI

A

crushing chest pain down left arm and jaw

86
Q

Anti-thrombolytic therapy usually uses

A

streptokinase: enzyme that dissolves blood clots or TPA

87
Q

Cardiac markers for AMI

A
  1. Myoglobin
  2. CK -> CK-2
  3. Cardiac troponin