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6-Clinical Nutrition 1 > Dyslipidemia and CVD Part 1 > Flashcards

Dyslipidemia and CVD Part 1 Flashcards

1
Q

What is the role of the cardiovascular system?

A
  • regulates blood flow to tissues (delivers 02 blood and nutrients, retrieves waste products)
  • thermogulation
  • hormone transport
  • maintenance of fluid volume
  • regulation of ph
  • gas exchange
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2
Q

What are the major forms of CVD?

A
  • HTN
  • Atherosclerosis
  • CHD
  • Peripheral Vascular Disease (Cerebrovascular Disease, Deep Vein Thrombosis)
  • CHF (congestive heart failure)
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3
Q

How is the atherosclerosis plaque form?

A
  • monocytes respond to injury on the artery wall, slip under blood vessel cells
  • engulf LDL cholesterol becoming foam cells
  • the thin layer of foam cells develop on artery walls form fatty streaks
  • a fatty streak thickens and forms plaque
  • plaque accumulates additional lipids, smooth muscle cells, connective tissue, and cellular debris
  • artery expands to accommodate the plaque making it more prone to rupture and thrombosis
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4
Q

What is atherosclerosis?

A

thickening of the blood vessel walls caused by presence of atherosclerotic plaque

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5
Q

Atherosclerosis results in _____

A

restriction of blood flow

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6
Q

Atherosclerosis is associated with _____

A
  • myocardial infarction (MI)
  • cerebrovascular accident (CVA, stroke)
  • peripheral vascular disease (PVD) –> impede with the venous return of the blood to heart
  • CHD
  • CHF when severe CHD or MI occurs
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7
Q

What is the pathophysiology of atherosclerosis?

A
  • complex and not well understood
  • involves endothelial cells, smooth muscle cells, platelets, and leukocytes
  • begins as a response to endothelial lining injury that results in an inflammatory process
  • results in restriction of arterial blood flow
  • asymptomatic until it progresses to ischemic heart disease
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8
Q

How does the damage to the arterial wall happens?

A
  • high blood pressure
  • chemicals from tobacco
  • oxidized LDL
  • glycated proteins
  • decreased NO
  • Angiotensin II
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9
Q

What is the normal range for total cholesterol levels

A

<5.2 mmol/L

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10
Q

What is the normal range for HDL

A

1.0 - 1.5 mmol/L

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11
Q

What is the normal range for LDL

A

<2.6 mmol/L

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12
Q

What is the normal range for TG

A

< 1.7 mmol/L

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13
Q

What are the risk factors for atherosclerosis?

A
  • risk factors have an additive effect
  • family history
  • age and sex (more common over age of 65 and in men)
  • obesity
  • dyslipidemia
  • physical inactivity
  • DM
  • impaired fasting glucose/metabolic syndrome
  • cigarette smoke
  • obstructive sleep apnea
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14
Q

What are the irreversible risk factors for atherosclerosis?

A
  • age
  • gender
  • genetics
  • familial history of CVD (1st relative, men<55y, 2nd relative women <65y)
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15
Q

What are the reversible risk factors for atherosclerosis?

A
  • diabetes
  • HTN
  • obesity
  • hyperlipidemia
  • atherogenic diet
  • smoking
  • lack of physical activity
  • low HDL (<1.0 mmol/L; <1.3 mmol/L women)
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16
Q

What are the functions of apoproteins?

A
  • synthesis and secretion of specific lipoproteins
  • stabilize surface coat of lipoproteins
  • activate enzymes (e.g. Apo C-II activates LPL)
  • interact with cell surface receptors
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17
Q

What is the major role of apoproteins on lipoproteins?

A

primary determinants of the metabolic fate of lipoproteins

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18
Q

What do apoproteins reflect in terms of lipoproteins?

A

reflect changes in lipoprotein composition

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19
Q

What do apoproteins indicate on plasma?

A

indicative of the number of lipoproteins in plasma (concentration)
- apoproteins may be better predictors of heart disease than lipid levels and may correlate with the severity of the disease

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20
Q

What are the major apoproteins found on chylomicrons?

A

B-48, E, A-1, A-IV, C-II, C-III

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21
Q

What are the major apoproteins found on VLDL?

A

B-48, C, E

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22
Q

What are the major apoproteins found on LDL?

A

B-100

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23
Q

What are the major apoproteins found on HDL?

A

A-1, A-2, C, E

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24
Q

What is the most frequent genotype that is seen of Apo-E?

A

E3/E3 (60%)

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25
Q

What is the problem with E2 genotype of ApoE?

A

does not react with ApoE receptor of LDL

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26
Q

How dyslipidemia classified?

A

primary and secondary

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27
Q

What is primary dyslipidemia?

A

single or poly-genetic abnormalities affecting lipoprotein function resulting in hyper or hypo lipidemia

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28
Q

How is primary dyslipidemia diagnosed?

A
  • history (age, onset, family members)
  • physical signs (e.g. xanthomas)
  • lab analysis: lipid profile, apoproteins, LPL activity
  • appearance of serum
  • genetic sequencing for rare cases
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29
Q

What is secondary dyslipidemia?

A

environmental causes +/- predisposition

  • due to other causes than genetic
  • more prevalent
  • may exacerbate primary dyslipidemia
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30
Q

What are the classes of primary hypolipoproteinemias?

A
  • Abetalipoproteinemia
  • Familial hypobetalipoproteinemia
  • Familial alpha-lipoprotein deficiency (Tangier disease)
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31
Q

What is abetalipoproteinemia?

A
  • hypolipoproteinemia
  • defect in apoporotein B synthesis
  • no chylo, VLDL, LDL formed and TAG accumulate in liver and intestine
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32
Q

What is Familial hypobetalipoproteinemia?

A
  • hypolipoproteinemia

- LDL concentration is 10-50% of normal but chylomicron formation occurs

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33
Q

What is Familial alpha-lipoprotein deficiency (Tangier disease)?

A
  • hypolipoproteinemia
  • virtual absence of HDL (Apo-A), CE accumulate in tissues
  • Chylo, VLDL, LDL are all normal
  • moderate hyper TG
34
Q

What are the 5 phenotypes of hyperlipoproteinemia?

A

Type I –> hyperchylomicronemia
Type IIa –> hypercholesterolemia
Type IIa, IIb, IV, or III –> combined hyperlipidemia
Type III –> endogenous hypertriglyceridemia
Type IV –> hypertriglyceridemia
Type V –> mixed hyperlipidemia

35
Q

Which type of hyperlipoproteinemia is the most common?

36
Q

What is the lipid abnormality of type I hyperlipoproteinemia (hyperchylomicronemia)?

A
  • increased TG

- decreased HDL

37
Q

What is the lipoprotein abnormality of type I hyperlipoproteinemia (hyperchylomicronemia)?

A

chylomicron

increased chylo fasting

38
Q

What are some clinical features of type I hyperlipoproteinemia (hyperchylomicronemia)?

A
  • early
  • xanthomas
  • abdominal pain
  • pancreatitis
  • lipemia
  • retinalis
39
Q

What is the lipid abnormality of type IIa hyperlipoproteinemia (hypercholesterolemia)?

A
  • increased LDL-C

- TG: N or H

40
Q

What is the lipoprotein abormality of type IIa hyperlipoproteinemia (hypercholesterolemia)?

41
Q

What are some clinical features of type IIa hyperlipoproteinemia (hyperchylomicronemia)?

A

vascular disease

42
Q

What is the lipid abnormality of combined hyperlipidemia?

A
  • increased cholesterol AND/OR
  • increased TG
  • decreased HDL-C
43
Q

What is the lipoprotein abnormality of combined hyperlipidemia?

A

IIb –> increased LDL +/- VLDL, apoB

III –> b-VLDL

44
Q

What are some clinical features of combined hyperlipidemia?

A
  • xanthomas
  • vascular disease
  • variable
45
Q

What are lipid abnormalities of type IV hyperlipoproteinemia (endogenous hyperTGemia)?

A
  • cholesterol N or H

- increased TG

46
Q

What is the lipoprotein abnormality of type IV hyperlipoproteinemia (endogenous hyperTGemia)?

47
Q

What are some clinical features of type IV hyperlipoproteinemia (endogenous hyperTGemia)?

A
  • Xanthomas
  • diabetes
  • obesity
  • alcohol
48
Q

What are the lipid abnormalitiess of type V hyperlipoproteinemia (mixed hyperlipidemia)?

A
  • Cholesterol N or H
  • Increased TG
  • decreased HDL-C
49
Q

What is the lipoprotein abnormality of type V hyperlipoproteinemia (mixed hyperlipidemia)?

A
  • high VLDL, chylomicrons present
50
Q

What are some clinical features of type V hyperlipoproteinemia (mixed hyperlipidemia)?

A

idem to I and IV

51
Q

What are the effects of obesity on lipoprotein metabolism?

A
  • increased substrate flux to liver
  • POSTPRANDIAL = due to excess calories (lipids and CHO)
  • POSTABSORPTIVE = due to high adipose tissue and hormones sensitive lipase (HSL) activity (bc of insulin resistance) resulting in increased FFA flux to liver
52
Q

How is obesity is related to HDL-C reduction?

A

BMI and Abdominal visceral fat

53
Q

How is BMI related to HDL-C reduction?

A
  • inverse relationship between BMI and HDL

- stronger association of BMI with HDL than LDL

54
Q

How is abdominal/visceral fat related to HDL-C reduction?

A
  • stronger association with HDL than total body fat

- stronger association in men and post-menopausal women

55
Q

How are TOT-CHOL, LDL-C, HDL-C affected by a diet high in cholesterol?

A

TOT CHOL = increases
LDL-C = increases
HDL-C = no change

56
Q

How are TOT-CHOL, LDL-C, HDL-C affected by a diet high in sat fats?

A

TOT CHOL = increases
LDL-C = increases
HDL-C = increases

57
Q

How are TOT-CHOL, LDL-C, HDL-C affected by a diet high in trans fats?

A

TOT CHOL = increases
LDL-C = increases
HDL-C = decreases

58
Q

How are HDL-C and TG affected by a diet high in sugars?

A 
HDL-C = decreases
TG = increases
59
Q

How are HDL-C and TG affected by alcohol?

A 
HDL-C = increases
TG = increases
60
Q

How are TOT-CHOL, LDL-C, HDL-C affected by smoking?

A

TOT CHOL = increases/no change
LDL-C = increases/no change
HDL-C = decreases

61
Q

How are HDL-C and TG affected by lack of physical activity

A 
HDL-C = decreases
TG = increases
62
Q

How are TOT-CHOL, LDL-C, HDL-C, TG affected by thiazide diuretics

A

TOT CHOL = increases
LDL-C = increases
HDL-C = increases/no change
TG = increases

63
Q

How are HDL-C and TG affected by beta blockers?

A 
HDL-C = decreases
TG = increases
64
Q

How are HDL-C and TG affected by obesity?

A 
HDL-C = decreases
TG = increases
65
Q

How does hypercholesterolemia occur in obesity?

A

total calories/increased saturated fa., cholesterol –> overproduction of VLDL particles –> VLDL-TG —> VLDL remnants –> Conversion to LDL –> reduced activity of LDL receptors –> accumulation in blood

66
Q

Why does HDL decrease in obesity?

A

increased catabolism of HDL by excess of adipose tissue

  • increased uptake of HDL 2 by adipocytes
  • increase clearance of apoA1 –> HDL catabolism
67
Q

What is the importance of apoproteins?

A
  • Primarydeterminantsofthemetabolicfateoflipoproteins
  • Reflectchangesinlipoproteincomposition
  • Indicative of # of lipoproteins in plasma (concentration)
  • Apoproteinlevelsmaybebetterpredictorsofheartdisease than lipid levels and may correlate with the severity of the disease
  • Aid in diagnostic of lipoprotein disorders and risk for developing CHD or CVD
68
Q

What is the main lipoprotein affected in type I hyperlipoproteinemia?

A

chylomicrons

69
Q

What is the specific marker of type I hyperlipoproteinemia?

A

absence or deficiency of LPL or apo C-II

70
Q

What is the main lipoprotein affected in type IIa hyperlipoproteinemia?

71
Q

What is the specific marker of type IIa hyperlipoproteinemia?

A

none (polygenic)

72
Q

What is the main lipoprotein affected in type IIb hyperlipoproteinemia?

A

LDL + VLDL

73
Q

What is the specific marker of type IIb hyperlipoproteinemia?

A

Mutation of LDL receptor or apo B

74
Q

What is the main lipoprotein affected in type III hyperlipoproteinemia?

75
Q

What is the specific marker of type III hyperlipoproteinemia?

76
Q

What is the main lipoprotein affected in type IV hyperlipoproteinemia?

77
Q

What is the specific marker of type IV hyperlipoproteinemia?

78
Q

What is the main lipoprotein affected in type V hyperlipoproteinemia?

A

chylo + VLDL

79
Q

What is the specific marker of type V hyperlipoproteinemia?

A

serum aspect: chylo band over VLDL

80
Q

What is Postprandial effect of obesity on lipoprotein metabolism?

A

due to excess calories (lipids and CHO)

81
Q

What is Postabsorptive effect of obesity on lipoprotein metabolism?

A

due to high adipose tissue and hormones sensitive lipase (HSL) activity (bc of insulin resistance) resulting in increased FFA flux to liver

6-Clinical Nutrition 1 (21 decks)

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