Clinical Biochemistry 02 - 03 - Diagnostics Of Lipid Disorders

Front 1

General objective of lipid control?

Back 1

Reduce CHD risk and prevent pancreatitis (in extreme cases of hypertriglyceridemias)

Front 2

Classification of lipid disorders

Back 2

1. Isolated hypercholesterolemia (mild--> moderate --> severe)
2. Isolated hypertriglyceridemia (mild--> moderate --> severe)
3. Mixed hyperlipidemia

Front 3

Effects of lipid level normalisation and the associated CHD risk? Basis for HDL relevance?

Back 3

1. In the LRC study a 9% cholesterol reduction resulted in an 18% decrease in CHD risk. Similar results were obtained in the Helsinki studies.
2. 2-3% reduction in CHD risk for every 1mg/dL of HDL. Both animal and regression studies support these findings.

Front 4

Most dangerous lipid disorder?

Back 4

1. Massive increase in LDL (which is rare)
2. High cholesterol/LDL and low levels of HDL is more common, and is almost dangerous

Front 5

Target value of lipids?

Back 5

>200mg/dL

Front 6

What is the most common dyslipidemia?

Back 6

Mixed dyslipidemia

Front 7

Lipid levels should be measured in?

Back 7

1. Those at risk (FHx, diabetes, etc)
2. All adults over 25, every 5th year. More frequent in smokers, obese people, diabetics, etc.

Front 8

Lipid target values for children?

Back 8

Cholesterol levels of:
1. <170mg/dL - Acceptable
2. 170-189mg/dL - Borderline
3. >200mg/dL - High

Front 9

In normal individuals, serum glycerol levels are negligible, however, in some patients these levels are really high. Which conditions may cause a high serum level of glycerol?

Back 9

1. Diabetes mellitus
2. Renal failure treated by hemodialysis

Front 10

What is the use of the cold flotation test?

Back 10

Distinguishes between TG elevation from dietary sources (TGs packed in chylomicrons) or if they're endogenous (VLDLs produced in the liver). A creamy top layer indicates nonfasting sample or deficit in lipoprotein lipase)

Front 11

How would you measure LDL levels indirectly?

Back 11

Friedewald's formula:
1. LDL-C=Total Cholesterol - HDL C - (triglycerides/5 [if mg/dL])
2. LDL-C=Total Cholesterol - HDL-C - (triglycerides/2.2 [if mmol/L])

Front 12

Substances or conditions that may interfere with cholesterol analysis?

Back 12

1. Bilirubin
2. Hemolysis
3. Lipemia
4. Ascorbic acid

Front 13

Drugs that are effective at lowering triglycerides and raising HDL?

Back 13

1. Nicotinic acid
2. Fibrates

Front 14

What is the HELLP syndrome?

Back 14

HELLP is an abbreviation of the three main features of the syndrome:
1. Hemolysis
2. Elevated Liver enzymes
3. Low platelet count

Front 15

Possible reasons for the increased morning levels of lipids?

Back 15

1. Increased lipolysis
2. Increased hepatic uptake of non-esterified fatty acids (NEFA)
3. Increased hepatic secretion of lipoproteins

Front 16

Total cholesterol levels vary with the menstrual cycle. At which point is the total cholesterol at a high? Low? What about VLDL?

Back 16

1. Highest seen in follicular phase
2. Lowest in the menstrual phase
3. Increase in VLDL and decrease in LDL during luteal phase (possibly owing to estrogen)

Front 17

Effect of surgery on lipid levels?

Back 17

Decrease in both cholesterol and triglyceride concentrations

Front 18

What effect does posture have on lipid levels?

Back 18

Serum cholesterol and triglyceride levels are higher when standing, differences being as much as 9%-19%

Front 19

Inheritance of familial hypercholesterolemia?

Back 19

AD

Front 20

What is Abetalipoproteinaemia?

Back 20

AR disorder, extremely low serum cholesterol levels. Malabsorption of lipids and fat soluble vitamins. Acantocytes in blood.

Front 21

HDL-modifying plasma enzymes and transfer proteins?

Back 21

1. LCAT
2. CETP
3. PLTP
4. Lipoprotein lipase
5. Hepatic lipase
6. Endothelial lipase

Front 22

What is "Fish Eye Disease"?

Back 22

Partial deficiency of LCAT

Front 23

What is Tangier disease?

Back 23

1. Familial alpha-lipoprotein deficiency.
2. AD inheritance, mutation in both alleles of ABC1

Front 24

Common findings in both types of LCAT deficiency?

Back 24

1. Markedly reduced HDL-C and apoA-I levels
2. Rapid catabolism of apoA-I and apoA-II
3. Corneal arcus
4. Premature atherosclerotic vascular disease

Front 25

Unique features of complete LCAT deficiency?

Back 25

Proteinuria and progressive renal insufficiency

Front 26

Inheritance of CETP deficiency?

Back 26

Autosomal co-dominant

Front 27

Features of CETP deficiency?

Back 27

1. Markedly elevated HDL-C and apoA-I levels
2. Delayed catabolism of HDL, HDL particles enlarged
3. No evidence of protection against atherosclerosis

Front 28

Inheritance of familial hyperlphalipoproteinemia?

Back 28

AD; molecular etiology unknown

Front 29

Features of familial hyperalphalipoproteinemia?

Back 29

1. Modest to marked elevations in HDL-C and apoA-I
2. Selective increased synthesis of apoA-I in some families
3. Assoiated with longevity and protection against atherosclerotic vascular disease

Front 30

Inheritance of hepatic lipase deficiency?

Back 30

AR

Front 31

In general, tests for specific genetic mutations are not performed in CAD. What are the reasons for this?

Back 31

1. It is not clear how much additional information will better treatment
2. The best way to avoid CAD is to modify lifestyle