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2.2 Clinical Chemistry > Lipids - Laboratory Tests > Flashcards

Lipids - Laboratory Tests Flashcards

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1
Q

What does a lipoprotein profile measure?

A

It measures the level of cholesterol in the blood

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2
Q

What are the two types of lipid profiles?

A

Fasting lipid profile

Random lipid profile

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3
Q

What tests may be included in a random lipid profile?
(2)

A

Triglycerides
Total cholesterol

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4
Q

What may be measured in the fasting lipid profile

A

HDL
LDL
Triglycerides
Total Cholesterol

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5
Q

What is the common method to detect cholesterol

A

CHOD-PAP method

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6
Q

What is the CHOD PAP method?
(5)

A

CHOD = cholesterol

P -> peroxidase

AP -> aminoantipyrine

It’s a coupled assay

It generates a coloured product, quinoneimine

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7
Q

What is the first reaction in the CHOD-PAP method

A

Cholesteryl Ester is converted to Free cholesterol and fatty acids by Cholesteryl Esterase

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8
Q

What converts cholesteryl esters to free cholesterol and fatty acids

A

Cholesteryl esterase

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9
Q

What is the second step in the CHOD-PAP assay

A

The free cholesterol + O2 is converted to 4-cholesten-3-one + H2O2 by cholesterol oxidase

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10
Q

What converts free cholesterol + O2 to 4-cholesten-3-one + H2O2?

A

Cholesterol oxidase

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11
Q

What is the third step of the CHOD-PAP assay?

A

2H2O2 + aminophenazone + phenol is converted into quinoneimine + 4H2O by peroxidase

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12
Q

What converts 2H2O2 + aminophenazone + phenol to quinoneimine + 4H2O?

A

Peroxidase

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13
Q

What is quinoneimine?

A

A red chromogen measured at 500nm

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14
Q

What does the cholesterol oxidase enzyme work on?
(2)

A

It accepts all sterols which have a 3B-hydroxyl group as substrates

Cholesterol is a 3B-hydroxy-cholest-5-ene

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15
Q

Give some examples of substrates for cholesterol oxidase

A

Plant sterols
Some steroid hormones
Cholesterol oxidation products

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16
Q

Why is the CHOD-PAP method considered biased?

A

Its biased towards slightly higher results compared to the definitive analysis method (isotope-dilution mass spectrometry)

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17
Q

What is the definitive analysis method for cholesterol

A

Isotope-dilute mass spectrometry

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18
Q

What are two alternative cholesterol assays other than the CHOD-PAP?

A

Lieberman-Burchard Reaction (CDC reference method)

Amplex red

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19
Q

Write about the Lieberman-Burchard reaction is a chemical method for cholesterol determination

A

Produces a blue-green colour with intensity proportional to the concentration of cholesterol

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20
Q

Why is the Lieberman-Burchard reaction?
(2)

A

Reagent is not very stable and it is best to use it fresh

The reagent also contains concentrated acids and is not particularly ‘user friendly’

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21
Q

Write about the amplex red assay
(4)

A

Similar to the CHOD-PAP method

CHOD is used to generate H2O2 but this is detected with amplex red rather than AAP

Amplex red is converted to the fluorescent resorufin in the presence of peroxidase and H2O2

More sensitive assay

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22
Q

List some variables in cholesterol testing
(5)

A

Age and gender -> males greater than females, this increases with age

Within day variation of between 2 and 3%

Seasonal variation of 3-5%

Venous stasis causing an increase between 10-15% within 5 minutes of stasis

Trauma can decrease lipid levels for several weeks

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23
Q

How are TAGs measured?
(3)

A

TAG ASSAY

A complex coupled assay with four separate enzyme reactions

It measures the concentration of free glycerol via generation of a quinoneimine product

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24
Q

What is the first step in the TAG ASSAT

A

Triglycerol + 3H2O

Converted to Glycerol + 3 fatty acids

By Lipase

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25
Q

What is the second step in the TAG assay

A

Glycerol + ATP

Converted to glycerol-3-phosphate + ADP

By Glycerol Kinase

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26
Q

What is the third step in the TAG Assay

A

Glycerol-3-phosphate + O2

Converted to Dihydroxyoxyacetone-P + H2O2

By Glycerol-P-Oxidase

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27
Q

What is the fourth step of the TAG assay

A

H2O2 + Aminophenazone + Chlorophenol

converted to Quinoemimine + HCL + 4H2O

By Peroxidase

28
Q

What are the four enzymes in the TAG Assay

A

Lipase
Glycerol Kinase
Glycerol-P-Oxidase
Peroxidase

29
Q

Why is investigation of lipoprotein important?

A

Due to the association of particular types of lipoprotein with cardiovascular disease

30
Q

How are lipoproteins investigates
(4)

A

Number of lipoprotein analysis e.g. NMR
Overall pattern of lipoproteins e.g. electrophoresis
Lipoprotein specific lipid content e.g. gel filtration
Apolipoprotein concentration e.g. ELISA

31
Q

How is HDL-Cholesterol specific lipid measurement measured?
(3)

A

Based on the use of reagents which cause LDL-Cholesterol to precipitate

In a fasting sample should only leave HDL-Cholesterol

Thus can use the normal assays on the supernatant and calculate the LDL as the difference between the Total Cholesterol and the HDL-C (Friedewald Formula)

32
Q

What is the Friedewald formula?

A

LDL Cholesterol = Cholesterol - (HDL + VLDL)

VLDL = TAG/2.2

33
Q

When can the Friedward Formula not be used to calculate LDL cholesterol

A

When the TAG is greater than 4.5 mmol/L

34
Q

How are normal ranges for lipids determined
(3)

A

Range depends on the populations

e.g. 20% higher cholesterol in Western populations vs Asian population

Levels change with age - gradual increase

35
Q

What are the normal recommendations for lipids?
(3)

A

Cholesterol should be less than 5 mmol/L

LDL-C should be less than 3.4 mM

TAG should be less than 1.5 mmol/L

36
Q

What does a risk assessment involve
(3)

A

Evaluate the risk of heart disease based on measurement of blood lipid levels

Algorithms of varying complexity evaluate the 10 year risk of an event

These risk assessments may inform the decision to start treatment

37
Q

Give six examples of factors measured in a risk assessment

A

Total cholesterol

HDL-C

LDL-C

TAG

Smoker

Blood pressure

38
Q

Define dyslipidemia
(2)

A

A consequence of abnormal lipoprotein metabolism

Lipid levels above the recommended levels

39
Q

What are the four types of dyslipidemia

A

Elevated Total Cholesterol

Elevated Low-density lipoproteins

Elevated triglycerides

Decreased High-density lipoproteins

40
Q

What are the two types of dyslipidaemia

A

Primary and secondary

41
Q

What is primary dyslipidaemia
(2)

A

Single or multiple gene mutation

Results in disturbances of LDL, HDL and TAG Production or clearance

42
Q

What is secondary dyslipidaemia?
(2)

A

Sedentary lifestyle

Excessive consumption of cholesterol - saturated fats and trans-fatty acids

43
Q

What is the common type of dyslipidaemia in Ireland

A

Secondary

44
Q

Give some examples of lipid abnormalities

A

Hypercholesterolaemia

45
Q

Why is hypercholesterolaemia dangerous?

A

Its a major risk factor for coronary heart disease

46
Q

How does hypercholesterolemia cause heart disease?

A

Cholesterol is deposited along walls of blood vessels

LDL is a key player in this process

Plaque ruptures and clot forms -> this impedes blood flow, tissues starved of oxygen and die which can cause angina or heart attack

47
Q

What are the main major risk factors for coronary heart disease?
(4)

A

Smoking
High blood pressure
High blood cholesterol
Physical inactivity

There are also some genetic components

48
Q

What is the most common classification system used for primary Hyperlipidemia?

A

Based on Fredrickson

Defined categories based on the spectrum of changes in blood lipids

49
Q

What is Fredrickson Type I primary hyperlipidemia
(4)

A

Chylomicron

Deficiency of lipoprotein lipase of apolipoprotein CII (which activates LPL)

An inability to clear chylomicrons from the circulation

Since chylomicrons are TAG rich it leads to profound hypertriglyceridemia

50
Q

What is a tell tale sign of Chylomicron Syndrome (Fredrickson Type I) Primary hyperlipidemia

A

High levels of chylomicron TAGs leads to hepatomegaly and eruptive xanthomata

The lipids essentially burst out of the skin

51
Q

How is Chylomicron Syndrom (Fredrickson Type I) Primary Hyperlipidemia syndrome treated?

A

Treated with a low fat diet

In ApoCII deficient forms plasma infusion may be used to temporarily replace ApoCII levels and thus LPL activity

52
Q

What is Fredrickson Type IIa Primary Hyperlipidemia also called?

A

Familial Hypercholesterolemia

53
Q

What causes FT IIa Primary Hyperlipidemia/ Familial Hypercholesterolemia
(6)

A

Deficiency of LDL-receptor function

Typically a mutation in the receptor

Can also have deficits in cytoplasmic adaptor proteins

This prevents LDL from being internalised i.e. it remains in plasma

1;500 people carry the mutation

LDL cannot be removed from the plasma

54
Q

What are some characteristic traits of FT IIa Primary Hyperlipidemia/ Familial Hypercholesterolemia?

A

Cholesterol levels elevated

TAG levels generally show minor changes

55
Q

What are some symptoms of FT IIa Primary Hyperlipidemia/ Familial Hypercholesterolemia?

A

Tendon Xanthoma

Corneal Arci

56
Q

How is FT IIa Primary Hyperlipidemia/ Familial Hypercholesterolemia treated

A

In heterozygous FH LDL-R is upregulated -> more receptors with residual function will cleave LDL from the blood

In homozygous FH may need plasma apheresis

57
Q

What is Fredrickson Type III called?

A

Hyperlipoproteinemia

58
Q

What causes hyperlipoproteinemia

A

Its associated with the E2 variant of APO-E

59
Q

What does FS Type III result in?
(4)

A

Impaired catabolism of IDL

IDL is not cleared as well from the plasma

Causes accumulation of VLDL remnants

It is often precipitated by conditions which increase VLDL

60
Q

What exactly happens in secondary hyperlipidemia

A

Diseases lead to increases in either cholesterol or TAG as a secondary effect

61
Q

Give some examples of secondary hyperlipidemias

A

Predominant hypercholesterolaemia

Predominant hypertriglyceridaemia

62
Q

What may cause prominant hypercholesterolaemia
(2)

A

Cholestasis

Primary hypothyroidism

63
Q

What may cause predominant hypertriglyceridemia?
(3)

A

Obesity
Diabetes
Metabolic Syndrome

64
Q

How is hypercholesterolemia treated
(3)

A

Therapies target cholesterol absorption or synthesis

Dietary intervention is essential - cut out saturated fats, eggs etc (absorption), use plant stanol enriched spreads (absorption)

Theres not much you can do from a dietary perspective to stop cholesterol synthesis -> drugs

65
Q

What drugs are used to treat hypercholesterolemia?
(4)

A

Drug therapies block either synthesis or absorption

Statin class of drugs competitively inhibit cholesterol synthesis -> lipitor, zocor

Eztimibe blocks cholesterol absorption (bile acid binding resin)

Can be used in combination

2.2 Clinical Chemistry (28 decks)

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