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mt > CC - LIPIDS 2 > Flashcards

CC - LIPIDS 2 Flashcards

1
Q

Transport of hepatic-derived lipids

A

Endogenous Pathway

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2
Q

IN Endogenous Pathway, ______ loses core lipids once secreted in the circulation

A

VLDL

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3
Q

Loss of core lipids leads to conversion of VLDL to _____

A

remnants

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4
Q

About half of the remnants are converted to ____, and half are taken in by the ____

A

LDL ; liver

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5
Q
  • Mediated by HDL
  • Excess cholesterol from peripheral cells is transported back to the liver
A

Reverse Cholesterol Transport Pathway

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6
Q

HDL serves to taxi cholesteryl esters to chylomicrons/VLDL remnants to liver

A

Reverse Cholesterol Transport Pathway

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7
Q

Conversion of cholesterol into bile acids for removal

A

Reverse Cholesterol Transport Pathway

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8
Q

Specimen Collection for Lipid Analysis

A
  1. Serum
  2. Fasting
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9
Q

preferred specimen

A

12 hour fast preferred

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10
Q

avoid _____, Presence of fat droplets suspended in a solution.

A

lipemia

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11
Q

Lipemia affects assays by affecting absorbance due to ______ of light

A

refraction

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12
Q

high plasma lipid concentrations can cause excessive plasma _____ and interfere with _________

A

turbidity ; spectrophotometric methods

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13
Q

Concentration differs between men, women and children due to ________. ______ and _______

A

sex hormone, concentration, and age

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14
Q
  • Higher HDL
  • Lower Cholesterol, triglyceride

is seen in

A

Women

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15
Q

As aging, Men and women increase in ______, _______ and ______

A

total cholesterol, LDL cholesterol and triglyceride

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16
Q

Colorimetric measurement procedures are less costly but are subject to ________ substances and may require _________ and ________

A

interfering ; extraction steps ; strong acids

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17
Q

Classical method

A

Liebermann-Burchard

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18
Q

Liebermann-Burchard is involved extraction & hydrolysis. Uses _____ & ______

A

sulfuric ; acetic acids

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19
Q

In Liebermann-Burchard, results in formation of a ______, proportional to the __________.

A

green color ; cholesterol concentration

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20
Q

Anything that affects HDL & LDL levels will affect cholesterol concentration-because these lipoprotein contain increased ______

A

cholesterol

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21
Q

______ level inversely affects cholesterol level

A

Thyroxine

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22
Q

hypothyroid associated with ________

A

hyper cholesterol

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23
Q

hyper thyroid associated with _______

A

hypo cholesterol

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24
Q

documented that post-menopausal women have increased LDL cholesterol

A

Estrogen

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25
Q

altered endocrine function resulting in increased cholesterol

A

Pregnancy

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26
Q

Other factors include ______, _______, ________, and _________

A

hepatitis, nephrotic syndrome, emotional stress and diabetes mellitus

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27
Q

Dextran sulfate or phosphotungstate acid with magnesium chloride precipitates LDL and VLDL lipoproteins

A

Precipitation Reaction

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28
Q

HDL left in the supernatant is tested using cholesterol assay. The answer represents the amount of HDL in the sample

A

Precipitation Reaction

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29
Q

Elevated triglyceride levels - level exceeds 400 mg/dL

A

Drawbacks

30
Q

Detergents or enzymes binds sites of VLDL and LDL particles. HDL is then left to react with colored products and can be measured

A

Homogeneous Reaction

31
Q

Dsiadvantages (Homogenous Reaction)

A

lacks specificity for HDL

32
Q

desirable range for HDL

A

> 60 mg/dL

33
Q

gray-area for HDL

A

40-59 mg/dL

34
Q

high risk level of HDL

A

< 40 mg/dL

35
Q
  • Enzymatic
  • Colorimetric
  • Involve the liberation of glycerol by lipase
A

Triglyceride Measurement Methods

36
Q

recommended triglyceride range

A

< 150 mg/dL

37
Q

triglyceride borderline high

A

150-199 mg/dL

38
Q

very high triglyceride level

A

> 500 mg/dL

39
Q

Friedewald estimation ( calculation ) is used for ___ measurement

A

LDL measurement

40
Q

Total Cholesterol, Total Triglycerides and HDL with routine procedure

Estimate the LDL with the following :
LDL= Chol- HDL -VLDL

and VLDL= Triglycerides/5

A

LDL Measurement

41
Q

stems from the deposition of lipids in artery walls.

A

Arteriosclerosis

42
Q

Result of malfunctions in the synthesis, transport or catabolism of lipoproteins

A

Hyperlipoproteinemia

43
Q

Elevated lipoprotein levels

A

Hyperlipoproteinemia

44
Q

Hyperlipoproteinemia divisions

A

/Hypercholesterolemia
/Hypertriglyceridemia
/Combined hyperlipidemia: elevation of cholesterol and triglyceride

45
Q
  • Linked to heart disease
  • Familial hypercholesterolemia (FH)
  • Genetic abnormality that predisposes people to high cholesterol levels, specifically LDL cholesterol.
  • Make cholesterol normally but lack or are deficient in active LDL receptors, so LDL builds up in the circulation .
  • Without the LDL receptors, LDL cannot be bound and cholesterol cannot be transferred into the cell
A

Hypercholesterolemia

46
Q
  • Imbalance between synthesis and clearance of VLDL in circulation
  • Deficiency of LDL or apo-C ( co-factor for LPL activity)
  • Chylomicrons cannot be cleared and triglycerides remain high
  • Normal function is for LDL to hydrolyze triglycerides carried in the chylomicrons and VLDL to give cells energy
A

Hypertriglyceridemia

47
Q

causes of Hypertriglyceridemia

A

genetic abnormalities such as Familial hypertriglyceridemia

48
Q

secondary causes of Hypertriglyceridemia

A

Hormonal abnormalities in pancreas, adrenals, pituitary and of diabetes mellitus

49
Q

Hypertriglyceridemia is Influenced by many hormones such as

A
  • Insulin, glucagon, pituitary growth hormone, adrenocorticotropic hormone (ACTH), thyrotropin, epinephrine, norepinephrine,
50
Q

Hormones trigger lipase can cause _____ and _______

A

acute and recurrent pancreatitis

51
Q
  • Presence of elevated levels of serum cholesterol and triglycerides
  • Results from accumulation of cholesterol-rich VLDL and chylomicron remnants from defective catabolism
  • Risk factor for CHD
  • Primarily congenital
A

Combined Hyperlipoproteinemia

52
Q

Low levels of lipoproteins

A

Hypolipoproteinemia

53
Q

2 forms of Hypolipoproteinemia

A
  1. Hypoalphalipoproteinemia
  2. Hypobetalipoproteinemia
54
Q
  • Decrease in circulating HDL (< 40 mg/dL)
  • Lack of hypertriglyceridemia
  • Due to a genetic defect (Tangier Disease)
A

Hypoalphalipoproteinemia

55
Q

Low levels of LDL cholesterol

A

Hypobetalipoproteinemia

56
Q

Absence of lipoproteins containing Apo-b

A

Abetalipoproteinemia

57
Q

Abetalipoproteinemia includes

A

LDL and VLDL

58
Q

Abetalipoproteinemia results in

A

Difficulty in weight gain and growth
Fat absorption problems
RBC membrane defects
Usually effects infants

59
Q

activate hormone-sensitive lipase in adipose tissue, thereby increasing the supply of fatty acids for oxidation in other tissues, and inactivate acetyl-CoA carboxylase.

A

Glucagon and Epinephrine

60
Q

regulates the levels of acetyl-CoA carboxylase and fatty acid synthase by controlling their rate of synthesis.

A

Insulin

61
Q

complete absence of HDL with very low levels of apoAI and apoAII due to inheritance of homozygous recessive alleles.

A

Tangier disease

62
Q

Tangier disease results to accumulation of cholesterol esters in

A

liver, spleen, lymph nodes, cornea, skin

63
Q

(Familial chylomicronemia)
– elevated chylomicron due to ineffective or
insufficient LPL

A

Fredrickson type 1

64
Q

(Primary hypercholesterolemia)
- increased LDL

A

Fredrickson type II

65
Q

(Familial dysbetalipoprotinemia)
- increased IDL

A

Fredrickson type III

66
Q

(Familial hypertriglyceridemia)
- increased VLDL

A

Fredrickson type IV

67
Q

markedly increased triglyceride

A

Fredrickson type V

68
Q

deficiency of β –glucocerebrosidase

A

Gaucher’s disease

69
Q

deficiency of sphingomyelinase

A

Niemann – Pick disease

70
Q

accumulation of galactocerebroside-β – galactosidase

A

Krabbe’s disease

71
Q

deficient α – galactosidase A

A

Fabry’s disease

72
Q

deficiency in hexosaminidase A

A

Tay-Sachs disease

mt (54 decks)

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