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LMP301 > LMP301 Lecture 6: Lipids & Cardiac Disease > Flashcards

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
Which is the largest lipoprotein?
CM
25
Purpose of CM
Transport TG and TC
26
What happens to the CM remnant?
Metabolized by the liver to give VLDL
27
Purpose of VLDL
Carry mostly TG and some TC to adipose & muscle tissues
28
What happens to VLDL during transfer?
Some of it's surface components are lost
29
VLDL ->
IDL
30
Purpose of IDL
1. Return to liver | 2. Become LDL
31
Purpose of LDL
Carries TC to peripheral tissues
32
What do LDL bind to?
Specialized receptors on liver & peripheral cells
33
Atherogenic
Promote formation of fatty plaques in the arteries
34
Which LP is atherogenic?
LDL
35
Statins try to lower...
LDL
36
HDL is composed of
proteins & phospholipids
37
Where is HDL made?
Liver
38
What happens to HDL during transport?
Accepts TC from other lipoproteins; increase in size (HDL-1 -> HDL-2 -> HDL-3)
39
Purpose of HDL
Carries TC from peripheral tissues to liver (for removal) using reverse cholesterol transport
40
What is the only organ that can excrete significant amounts of cholesterol?
Liver
41
How does the liver excrete cholesterol?
Bile salts
42
Importance of bile salts?
Absorbs fat-soluble vitamins in the intestine
43
2 types of lipid disease
1. Inherited (genetic factors) | 2. Acquired (risk factors)
44
Familial hypercholesterolemia
High levels of cholesterol
45
FHC
Familial hypercholesterolemia
46
Familial hypertriglyceridemia
Genetic mutations that cause high levels of triglycerides
47
2 types of inherited lipid disease
1. FHC 2. Familial hypertriglyceridemia Combination of 1 and 2.
48
Causes of FHC
Defect in LDL receptor: LDL is unable to return to liver, so excess amount circulates in the blood
49
Risk for those w/ heterozygous FHC gene
have MI in their 30's | 1:500 people
50
Risk for those homozygous for FHC gene
have MI in childhood (1:1000000)
51
Marker for FHC
Xanthoma
52
Xanthoma
Build-up of fatty deposits in soft tissues (e.g. eyelids)
53
Thrombosis
When the fibrous cap breaks and ruptures the artery, blood clot that forms at the site of damage will clog the artery
54
How to treat MI and stroke surgically?
Busters: 1. Enzymes that break the clot 2. Balloons to open up the vessel
55
Pathogenesis of IHD
1. Oxidant status 2. Inflammatory response markers 3. Lipoprotein(a)
56
Oxidant status
LDL in lipid plaque become oxidized by free radicals.
57
Marker for oxidant status
Homocysteine in some patients (reducing AA)
58
Inflammatory response markers
Tissue damage at atheroma triggers inflammatory response. | Oxidation of LDL also triggers inflammatory response
59
Marker for inflammatory response?
CRP
60
CRP
C-reactive protein
61
C-reactive protein
Acute phase reactant (appears quickly) when body has an inflammation. Used to identify those at higher risk for IHD.
62
Role of Lp(a) in IHD
Interfere with plasminogen process. | Plasminogen is anti-clotting factor, so Lp(a) causes clotting to happen.
63
How to prevent IHD?
1. Routine screening of cholesterol after the age of 40 | 2. If screen shows problems: fasting lipid profile
64
TC =
LDL + HDL + VLDL
65
VLDL =
TG / 2.2 (MUST BE FASTING)
66
LDL =
TC - (HDL + TC/2.2)
67
Which lipoprotein is usually calculated? What conditions must be met?
LDL-C | TG must be less than 4.5 mmol/L
68
Lipid indicators of risk for IHD
1. TC : HDL ratio 2. Apo-B 3. Apo-A1
69
Apo-B is a marker for...
``` VLDL IDL LDL Lp(a) (1:1 ratio) ```
70
Apo-B might be more useful in patients with...
metabolic syndrome
71
Apo-A1 is a marker for...
HDL | 1:1 ratio
72
Benefit of measuring Apo-B and A1 over lipid profile
NO need to fast
73
Problems with cholesterol screening
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
Framingham heart study
Model for 10-year risk of coronary artery disease (guildline for heart disease risk factors). ATP-III is the treatment guidelines developed.
75
What automatically puts you at high risk for IHD?
Diabetes II
76
Risk factors associated with IHD from the Framingham heart study
1. Age 2. HDL 3. TC 4. BP 5. Smoker 5. Diabetes 6. Sex
77
10-year risk score
Points that = some level of risk for developing CVD in the next 10 years
78
Risk categories from the 10-year risk score
High, moderate, low
79
Metabolic syndrome (X)
A cluster of risk factors that are associated with heart disease & diabetes. Getting 3 or more of those factors = metabolic syndrome
80
Key metabolic changes (metabolic syndrome)
1. Impaired fasting glucose (Insulin-resistance) | 2. Abdominal fat (small-dense LDL)
81
management of IHD
1. TLC: therapeutic lifestyle changes 2. Drugs 3. CABG: coronary artery bypass graft
82
2 TLC changes to manage IHD
1. Exercise | 2. Vegetarian diet
83
CABG
Vein grafted: replace coronary artery
84
AMI
Acute Myocardial infarction
85
Symptom for AMI
crushing chest pain down left arm and jaw
86
Anti-thrombolytic therapy usually uses
streptokinase: enzyme that dissolves blood clots or TPA
87
Cardiac markers for AMI
1. Myoglobin 2. CK -> CK-2 3. Cardiac troponin

LMP301 (18 decks)

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