LMP301 Lecture 6: Lipids & Cardiac Disease Flashcards Preview

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Flashcards in LMP301 Lecture 6: Lipids & Cardiac Disease Deck (88)
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Ischemic heart disease

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

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IHD

Ischemic heart disease

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____ of deaths from IHD can be prevented

>1/2

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Differences between men and women in terms of IHD

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

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Disease that may result from fat deposits in the arteries

1. IHD
2. Cerebrovascular disease
3. Peripheral vascular disease

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Cerebrovascular disease

Stroke

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Peripheral vascular disease

Blood can't flow the the extremeties

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Where is the lipid core found?

Nested in the intima

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What holds the lipid core in place?

Fibrous cap

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4 types of lipids

1. Cholesterol
2. Triglycerides
3. Phospholipids
4. FA

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Which lipids are used for fule?

TG and FA

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Which lipids can be found in the membrane?

Cholesterol & phospholipids

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Functions of cholesterol

Production of hormones
Membrane structure

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Functions of phospholipids

Make up cell membranes
Signalling

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Transporter for lipids

Lipoproteins carry circulating lipids in plasma & lympth

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Carriers for FFA

Albumin

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Exogenous pathway for lipids

Lipids consumed from fats

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Endogenous pathway for lipids

Lipids made by the body

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Outline exogenous pathway for lipid metabolism

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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Outine endogenous pathway of lipid metabolism

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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Extra-hepatic cells

Cells other than liver cells

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What does HDL do?

Reverse cholesterol transport

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Reverse cholesterol transport

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

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List the lipoproteins in order of least dense -> most

1. Chylomicrons
2. VLDL
3. IDL
4. LDL
5. HDL

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Which is the largest lipoprotein?

CM

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Purpose of CM

Transport TG and TC

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What happens to the CM remnant?

Metabolized by the liver to give VLDL

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Purpose of VLDL

Carry mostly TG and some TC to adipose & muscle tissues

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What happens to VLDL during transfer?

Some of it's surface components are lost

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VLDL ->

IDL

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Purpose of IDL

1. Return to liver
2. Become LDL

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Purpose of LDL

Carries TC to peripheral tissues

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What do LDL bind to?

Specialized receptors on liver & peripheral cells

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Atherogenic

Promote formation of fatty plaques in the arteries

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Which LP is atherogenic?

LDL

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Statins try to lower...

LDL

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HDL is composed of

proteins & phospholipids

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Where is HDL made?

Liver

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What happens to HDL during transport?

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

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Purpose of HDL

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

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

Liver

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How does the liver excrete cholesterol?

Bile salts

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Importance of bile salts?

Absorbs fat-soluble vitamins in the intestine

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2 types of lipid disease

1. Inherited (genetic factors)
2. Acquired (risk factors)

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Familial hypercholesterolemia

High levels of cholesterol

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FHC

Familial hypercholesterolemia

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Familial hypertriglyceridemia

Genetic mutations that cause high levels of triglycerides

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2 types of inherited lipid disease

1. FHC
2. Familial hypertriglyceridemia

Combination of 1 and 2.

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Causes of FHC

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

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Risk for those w/ heterozygous FHC gene

have MI in their 30's
(1:500 people)

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Risk for those homozygous for FHC gene

have MI in childhood (1:1000000)

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Marker for FHC

Xanthoma

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Xanthoma

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

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Thrombosis

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

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How to treat MI and stroke surgically?

Busters:
1. Enzymes that break the clot
2. Balloons to open up the vessel

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Pathogenesis of IHD

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

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Oxidant status

LDL in lipid plaque become oxidized by free radicals.

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Marker for oxidant status

Homocysteine in some patients (reducing AA)

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Inflammatory response markers

Tissue damage at atheroma triggers inflammatory response.
Oxidation of LDL also triggers inflammatory response

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Marker for inflammatory response?

CRP

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CRP

C-reactive protein

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C-reactive protein

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

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Role of Lp(a) in IHD

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

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How to prevent IHD?

1. Routine screening of cholesterol after the age of 40
2. If screen shows problems: fasting lipid profile

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TC =

LDL + HDL + VLDL

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VLDL =

TG / 2.2 (MUST BE FASTING)

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LDL =

TC - (HDL + TC/2.2)

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

LDL-C
TG must be less than 4.5 mmol/L

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Lipid indicators of risk for IHD

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

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Apo-B is a marker for...

VLDL
IDL
LDL
Lp(a)
(1:1 ratio)

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Apo-B might be more useful in patients with...

metabolic syndrome

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Apo-A1 is a marker for...

HDL
(1:1 ratio)

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Benefit of measuring Apo-B and A1 over lipid profile

NO need to fast

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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

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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.

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What automatically puts you at high risk for IHD?

Diabetes II

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Risk factors associated with IHD from the Framingham heart study

1. Age
2. HDL
3. TC
4. BP
5. Smoker
5. Diabetes
6. Sex

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10-year risk score

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

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Risk categories from the 10-year risk score

High, moderate, low

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Metabolic syndrome (X)

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

Getting 3 or more of those factors = metabolic syndrome

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Key metabolic changes (metabolic syndrome)

1. Impaired fasting glucose (Insulin-resistance)
2. Abdominal fat (small-dense LDL)

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management of IHD

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

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2 TLC changes to manage IHD

1. Exercise
2. Vegetarian diet

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CABG

Vein grafted: replace coronary artery

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AMI

Acute Myocardial infarction

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Symptom for AMI

crushing chest pain down left arm and jaw

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Anti-thrombolytic therapy usually uses

streptokinase: enzyme that dissolves blood clots or TPA

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Cardiac markers for AMI

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