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Liz's Clinical Chemistry Module 2 > Lipids > Flashcards

Lipids Flashcards

1
Q

Three hepatic receptors to which LDL may bind to return cholesterol esters back to the liver in reverse cholesterol transfer pathway

A
  1. LDL receptor
  2. HDL receptor
  3. Remnant receptor
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2
Q

Electrophoretic pattern of Type V

A

Type I + Type IV; increased chylomicron band and pre-beta band

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3
Q

(At least) two risk factors of the metabolic syndrome

A
  1. BMI > 25
  2. Family history of diabetes mellitus
  3. History of gestational diabetes
  4. Polycystic ovary syndrome
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4
Q

Plasma apperance of Type III

A

Slightly cloudy to cloudy plasma

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5
Q

Mechanism to maintain cholesterol balance; LDL receptors deliver intact particles to lysosomes where cholesterol esters are hydrolyzed by lysosomal aicd lipase; associated apolipoproteins are degraded to small peptide and amino acid

A

Purpose of intraceullular-cholesterol transport pathway of lipid metabolism

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6
Q

List 5 analytes used to predict risk for development of CAD

A
  1. Apo B-100 (on LDL)
  2. Apo E
  3. Homocysteine
  4. High sensitivity CRP (hsCRP)
  5. Lipoprotein
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7
Q

Electrophoretic pattern of Type IIb

A

LARGE beta band

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8
Q

Three intracellular uses of cholesterol esterase

A

Membrane biogenesis, stored in intracellular lipid drops after re-esterification by ACAT catalysis

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9
Q

Major carrier of endogenous (hepatic origin) lipids

A

VLDL

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10
Q

Secretion of triglycerides from intestine

A

B-48

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11
Q

The importance of LPL and apo C-II in the formation of the VLDL remnant in the endogenous pathway

A

C-II activates LPL on the surface of endothelial cells, leading to TGL hydrolysis and free fatty acids release to peripheral cells

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12
Q

Elevated VLDL and chylomicrons, cholesterol increased, moderately increased TGL, LDL and HDL normal to low

A

Mixed Hyperlipoproteinemia/Type V

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13
Q

Elevated TGL w/o significantly increased cholesterol would cause increases in which two lipoproteins?

A

VLDL and chylomicrons

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14
Q

The formation of LDL in the endogenous pathway

A

IDL transfers apo E, C, free cholesterol, and phospholipids to HDL in the circulation making LDL

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15
Q

Three signs and symptoms of the metabolic syndrome

A
  1. Central obesity
  2. Hypertension
  3. High blood glucose
  4. High TGL
  5. Low HDL
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16
Q

Explain the process of dietary triglyceride metabolism

A
  • Digested in the duodenum and absorbed in proximal ileum

- Pancreatic and intestinal lipase and bile acids hydrolyze triglycerides to glycerol, monoglycerides, and fatty acids

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17
Q

Specific concentrations of TGL

- Desirable

A

< 150 mg/dL

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18
Q

Electrophoretic pattern of Type IIa

A

Increased beta band on electrophoresis

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19
Q

The effect of excess intracellular cholesterol on the cell

A

Downgrades HMG-CoA reductase activity, inhibits expression of LDL receptor, induces the synthesis of proteins involved in reverse cholesterol transport

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20
Q

HDL cholesterol precipitation methods

A
  1. Precipitate apo B-containing lipoproteins
  2. Centrifuge and analyze supernatant (HDL)
  3. Use direct assay to mask non-HDL fractions so they don’t react w/ enzymes used to measure cholesterol
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21
Q

The importance of apolipoprotein C-II and LPL for TGL hydrolysis in exogenous pathway

A

C-II activates LPL causing rapid hydrolysis of TGL into free fatty acids to be taken up by adipose or muscle cells

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22
Q

Lack proper forms of apo E to allow liver to identify chylomicron remnants and IDL, diagnosed at age 20 or higher, increased total cholesterol and TGL, normal to decreased LDL, increased IDL

A

Dysbetalipoproteinemia/ Type III

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23
Q

Electrophoretic pattern of Type I

A

Intense band at point of application or at chylomicrons

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24
Q

The specific site in the intestine where chylomicrons are assembled in the exogenous pathway

A

Intestinal epithelial cells

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25
Q

Four detrimental effects of oxidized LDL

A
  1. Macrophages are transformed into foam cells
  2. Cytotoxic effects are exerted on endothelial cells
  3. Platelet activation is increased
  4. Migration and proliferation of smooth muscle cells stimulated
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26
Q

How the chylomicron remnant is formed in the exogenous pathway

A

What remains of free fatty acids to enter the liver (Cholesterol esters) (B-48 and Apo E)

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27
Q

VLDL

  • % TGL
  • % Phospholipids
  • % Cholesterol
  • % Protein
  • Apolipoproteins
A
  • 55% TGL
  • 18% phospholipid
  • 19% cholesterol
  • 8 % protein
  • apo B-100, C-I, C-II, C-III, E
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28
Q

Genetic disorder in which there is a defect in synthesis or secretion of lipoproteins containing apo B; LDL is absent in homozygotes; total cholesterol usually < 30 mg/dL

A

Abetalipoproteinemia

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29
Q

Specific concentrations of LDL

- High

A

160-189 mg/dL

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30
Q

Fat absorption problems causing failure to thrive in infancy, mental and physical retardation, blindness, and acanthocytes on PBS

A

Abetalipoproteinemia

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31
Q

(At least) five modifiable risk factors for coronary artery disease

A
  1. Hypertension
  2. Smoking
  3. Obesity
  4. Diet
  5. Alcohol
  6. Stress
  7. High lipids
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32
Q

Basic structure of cholesterol

A

A steroid alcohol w/ 27 carbon atoms arranged in a tetracyclical sterane ring system

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33
Q

Total cholesterol 40-125 mg/dL, normal to elevated TGL, familial severe HDL and apo A-I deficiency, hyperplastic orange-yellow tonsils and adenoids plus hepatosplenomegaly

A

Hypoalphalipoproteinemia (Tangier disease)

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34
Q

Specific concentrations of TGL

- Very high risk

A

> =500 mg/dL

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35
Q

Transports dietary lipids that are absorbed by the intestine to the liver and peripheral tissues; TGL digested in duodenum and proximal ileum through action of pancreatic and intestinal lipases and in the presence of bile acids

A

Purpose of the exogenous pathway for dietary lipids

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36
Q

Empirical formula and three sources of fatty acids

A

R-COOH

  1. Diet (largest source)
  2. Adipose tissue
  3. Biosynthesis of all but the “essential fatty acids”
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37
Q

Discuss progression from fatty streaks to fibrous plaques to complicated lesions in atherosclerosis

A

Plaque deposited in blood vessels, inflammation allows lipids to come in and start consuming fat (foam cells), lumen decreases, accumulation of fibrous cap, then platelet thrombosis and fibrin deposits creating a necrotic core w/ debris

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38
Q

Three uses of intracellular cholesterol hepatocytes

A

Repackaged and secreted on lipoproteins converted to bile salts; directly secreted into bile

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39
Q

Specific appearance of serm/plasma w/ expected CHOL or TGL concentrations
- Normal TGL

A

Clear

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40
Q

Electrophoretic mobilities of LDL

A

Beta region

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41
Q

Specific appearance of serm/plasma w/ expected CHOL or TGL concentrations
- TGL > 500 mg/dL

A

Opaque/milky

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42
Q

Core of nonpolar, neutral lipids surrounded by more polar amphipathic lipids on the surface, contains one or more specific proteins; DIAGRAM IN LECTURE

A

Structure of lipoproteins

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43
Q

Common disorder, elevated VLDL, elevated LDL, increased total cholesterol, increased TGL

A

Combined hyperlipoproteinemia/Type IIb

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44
Q

Facilitates uptake of chylomicron remnant and IDL

A

Apo E

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45
Q

Specific concentrations of TGL

- Borderline

A

150-199 mg/dL

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46
Q

Macrophages accumulate excess cholesterol and become these (atherogenic)

A

Foam cells

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47
Q

The importance of apo E for hepatic uptake of the chylomicron remnant in the exogenous pathway

A

Required for hepatic endocytosis (entrance into the liver)

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48
Q

Describe the catabolic process of beta-oxidation

A

Shortens fatty acid chain from carboxyl end of molecule to form acetyl-CoA; condensed w/ oxaloacetate to form citrate to enter the Kreb’s cycle (yields more energy than catabolism at glucose)

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49
Q

Reagents used in enzymatic cholesterol methods

A

Cholesterol esterase and oxidase

50
Q

Specific concentrations of LDL

- Near/above optimal

A

100-129 mg/dL

51
Q

Six harmful effects of trans fatty acids

A
  1. Not recognized by enzymes
  2. If incorporated into cell membrane, membrane is more dense and function is altered
  3. Raises LDL and triglycerides
  4. Lowers HDL
  5. Increases risk of cardiovascular disease
  6. Has a detrimental effect on brain/nervous system
52
Q

Plasma appearance in Type IIb

A

Slightly turbid

53
Q

Activates LCAT

A

A-IV, C-1

54
Q

Describe the basic structure and the major function of triglycerides

A

3 fatty acids attached to glycerol;

major function: storage of fat in the tissues

55
Q

Enzyme deficiency and typical symptoms of Tay-Sachs disease

A

Deficiency: hexosaminidase
Symptoms: psychomoter deterioration, dementia

56
Q

Six functions of phosphoglycerides

A
  1. Components of cell membranes
  2. Enzyme activators
  3. Metabolic fuels
  4. Signaling molecules
  5. Surfactant
  6. Component of lipoproteins
57
Q

Reagents used in Liebermann-Burchard method

A

Sulfuric acid, acetic anhydride

58
Q

Specific concentrations of low value of HDL cholesterol

A

< 40 mg/dL

59
Q

Friedewald formular to calculate LDL concentration

A

LDL = TC– (VLDL + HDL); VLDL = TGL/5

60
Q

Autosomal recessive, usually detected before 10 years of age, TGL levels usually >1000, elevated chylomicrons only

A

Hyperchylomicronemia/Type I

61
Q

Chylomicrons

  • % TGL
  • % Phospholipids
  • % Cholesterol
  • Apolipoproteins
A
  • 86% TGL
  • 7% phospholipids
  • 5% cholesterol
  • apo A-I, A-IV, B-100, B-48, C-I, C-II, C-III, E
62
Q

Importance of emulsification of cholesterol

A

Necessary to solubilize cholesterol before absorption, this occurs by the formation of mixed micelles

63
Q

Reagents used in Abell method

A

Cholesterol esters chemically hydrolyzed then perform Liebermann-Burchard

64
Q

Five patient preparation instructions for proper lipid study specimen collections

A
  1. 12-14 hour fast (water only)
  2. Habitual diet and activity
  3. Stable weight over past 4 weeks
  4. No acute/recent illness, injury, or surgery (MI or CABG)
  5. No lipid-raising or lipid-lowering drugs
  6. Repeat in 1-4 weeks to diagnose
65
Q

(At least) five non-modifiable risk factors for coronary artery disease

A
  1. Gender
  2. Age
  3. Family history
  4. Race
  5. Diabetes mellitus
66
Q

Four functions of lipoproteins

A
  1. Facilitate direct cellular uptake and catabolism of lipoproteins
  2. Serve as structural component
  3. Serve as cofactor to regulate enzymes
  4. Facilitate transfer of lipids b/w lipoproteins
67
Q

5 general functions of lipids

A
  1. Serve as hormones or hormone precursors
  2. Aid in digestion
  3. Provide energy storage and metabolic fuels
  4. Provide functional and structural components in biomembranes
  5. Form insulation to prevent heat loss or to allow nerve conduction
68
Q

Pumps cholesterol out of the cells in the reverse-cholesterol transfer pathway

A

ABCA-1 transporter

69
Q

Electrophoretic mobilities of chylomicrons

A

At point of application

70
Q

Markedly elevated VLDL, normal LDL, increased TGL, normal cholesterol; deficiency of LPL or apo C-II

A

Hyperprebetalipoproteinemia/Type IV

71
Q

Genetic disorder, LDL concentrations about 1/10 of normal, total plasma cholesterol may be < 30 mg/dL, normal TGL

A

Hypobetalipoproteinemia

72
Q

Purpose is to remove excess cholesterol from peripheral cells and return it to the liver for excretion; mediated by HDL

A

Reverse cholesterol transport pathway of lipid metabolism and the lipoprotein that mediates it

73
Q

Electrophoretic pattern of Type III

A

Broad beta band of abnormal composition

74
Q

Electrophoretic mobilities of HDL

A

Alpha1 region (moves fastest to anode)

75
Q

Cofactor of LCAT

A

A-I

76
Q

Function and different sites of action for lecithin-cholesterol acyltransferase (LCAT) and acylocholesterol acyltransferase (ACAT)

A

Both reduce cytoxicity of free cholesterol
LCAT: extracellularly
ACAT: intracellularly

77
Q

Thickening, hardening, and loss of elasticity in artery walls

A

Arteriosclerosis

78
Q

The importance of apo B-100 in the intracellular-cholesterol transport pathway

A

LDL is recognized by LDL receptor

79
Q

Purpose is to transfer hepatic-derived lipids, especially TGLS, to peripheral cells for energy metabolism

A

Endogenous pathway for lipids

80
Q

Specific concentrations of total CHOL

- Desirable

A

< 200 mg/dL

81
Q

Specific concentrations of TGL

- High risk

A

200-499 mg/dL

82
Q

Specific concentrations of LDL

- Optimal

A

<100 mg/dL

83
Q

Secretion of triglycerides from liver binding protein to LDL receptor

A

B-100

84
Q

Intracellular enzyme responsible for cholesterol ester hydrolysis in the intracellular-cholesterol transport pathway

A

Lysosomal acid lipase

85
Q

HDL

  • % TGL
  • % Phospholipids
  • % Cholesterol
  • % Protein
  • Apolipoproteins
A

~50% protein (“high density”)
~50% lipids (~4% TGL, ~30% phospholipids, ~16% cholesterol esters)
- apo A-I and A-II

86
Q

Two functions of cholesterol

A

Helps organize cell membranes and controls permeability

87
Q

Plasma appearance of Type IV

A

Slightly cloudy, cloudy, or opaque

88
Q

Specific concentrations of total CHOL

- High

A

> =240 mg/dL

89
Q

The importance of the presence of only apo B-100 on LDL in the endogenous pathway

A

B-100 is the receptor protein that allows LDL to bind to hepatic or extrahepatic cells to deliver its cholesterol load

90
Q

Specific concentrations of LDL

- Very high

A

> =190 mg/dL (VERY BAD)

91
Q

The importance of mixed micelle formation in the absorption of dietary cholesterol in the exogenous pathway

A

Bile acids act as detergents; helps to transport cholesterol easily to epithelial cells to be absorbed

92
Q

Plasma appearance of Type IIa

A

Clear/orange

93
Q

Disposition of fatty acids after TGL hydrolysis in exogenous pathway

A

Free fatty acids combine w/ ALB and are taken up by muscle cells as an energy source or by adipose cells for energy storage as TGL

94
Q

Specific concentrations of total CHOL

- Borderline high

A

200-239 mg/dL

95
Q

TGL concentration above which the Friedewald formula is invalid

A

TGL > 400 mg/dL5

96
Q

Electrophoretic mobilities of VLDL

A

Pre-beta region

97
Q

The formation of IDL in the endogenous pathway

A

Progressive lipolysis of TGL from the core of VLDL transforms it to IDL

98
Q

Specific appearance of serm/plasma w/ expected CHOL or TGL concentrations
- Increased CHOL/TGL

A

Orange/yellow tint

99
Q

Specific concentrations of LDL

- Borderline high

A

130-159 mg/dL

100
Q

Importance of esterification of cholesterol

A

In order to reduce the cytotoxicity of free cholesterol

101
Q

A form of arteriosclerosis caused by focal accumulation of lipids, complex CHOs, blood, fibrous tissue, and calcium

A

Atheroscloerosis

102
Q

Specific appearance of serm/plasma w/ expected CHOL or TGL concentrations
- TGL 200-499 mg/dL

A

Hazy/turbid

103
Q

Specific concentrations of high HDL cholesterol

A

> =60 mg/dL (GOOD)

104
Q

Elevated LDL, normal TGL, increased cholesterol (800-1200 mg/dL), 3 variant forms

A

Hyperbetalipoproteinemia/Type IIa

105
Q

Electrophoretic pattern of Type IV

A

Increased pre-beta band

106
Q

Four reasons why HDL is considered “good” cholesterol

A
  1. Anti-clotting properties
  2. Promotion of the efflux of excess cellular cholesterol
  3. Antioxidant properties
  4. Anti-inflammatory properties
107
Q

Elevated cholesterol w/o increased TGL may be due to increases in which three lipoprotein fractions?

A

LDL, IDL, and VLDL

108
Q

Enzyme deficiency and typical symptoms of Niemann-Pick syndrome

A

Deficiency: sphingolyelinase
Symptoms: hearing problems, psychiatric problems, epilepsy, dysphagia, ataxia, learning difficulties, clumsiness

109
Q

Cofactor of LPL

A

C-II

110
Q

IDL

  • % TGL
  • % Cholesterol
  • % Protein
  • % Phospholipids
  • Apolipoproteins
A
  • 23% TGL
  • 37% cholesterol
  • Intermediate concentrations of lipid and protein b/w VLDL and LDL
  • apo B-100 and E
111
Q

Three important pancreatic enzymes and their substrates in the exogenous pathway for dietary lipids

A

Lipase, cholesterol esterase, and phospholipase A

112
Q

Three fat-soluble vitamins (terpenes)

A

Vitamins A, E, K

113
Q

Form the major lipids of cell membranes, increase rigidity, act as signal transducers in CNS, made by all cells except erythrocytes

A

Sphingolipids

114
Q

The importance of cholesterol ester transfer protein (CETP) in TGL cholesterol exchange

A

Removes TGL from LDL and exchanges it for cholesterol esters from HDL; LDL is rich in cholesterol esters and contain ONLY B-100

115
Q

Enzyme deficiency and typical symptoms of Gaucher’s disease

A

Deficiency: beta-glucocerebrosidase
Symptoms: Hepatomegaly, bone pain and crisis, collapsed vertebrae, splenomegaly, thrombocytopenia, anemia, osteonecrosis, osteopenia, Erlenmeyer flask deformity

116
Q

Plasma appearance of Type I

A

Creamy layer over clear plasma

117
Q

Hydrophilic adaptation in order to transport hydrophobic lipids to tissues and organs

A

Function of lipoproteins

118
Q

The major carrier of exogenous (dietary) lipids

A

Chylomicrons

119
Q

Inhibits C-II activation of LPL

A

C-III

120
Q

Why is it important that nascent HDL be converted to its spherical form (HDL2)?

A

So it can return to circulation to pick up more cholesterol

121
Q

LDL

  • % TGL
  • % Phospholipids
  • % Cholesterol
  • % Protein
  • Apolipoproteins
A
  • 6% TGL
  • 20% phospholipid
  • 50% cholesterol
  • 20% protein
  • ONLY apo B-100
122
Q

Plasma apperance of Type V

A

Opaque w/ floating creamy layer; “cottage cheese over milk”

Liz's Clinical Chemistry Module 2 (9 decks)

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