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Clinical Nutrition 1 > Dyslipidemia Part 1 > Flashcards

Dyslipidemia Part 1 Flashcards

1
Q

Thiazide diuretics

A

Increase TC
Increase LDL
Increase/same HDL
Increase TG

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2
Q

B-blockers

A

Decrease HDL

Increase TG

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3
Q

Corticosteroids

A

Increase ALL lipid (including HDL)

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4
Q

Estrogens

A

Decrease TC and LDL

Increase HDL and TG

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5
Q

Benzodiazepine

A

Increase TG

Decrease HDL

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6
Q

Retinoic acid

A

Increase TC, LDL, TG, decrease HDL

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7
Q

Antiretroviral

A

Increase TG

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8
Q

Diabetes

A

Increase TC, LDL, TG

Decrease HDL

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9
Q

Hypothyroidism

A

Increase TC, LDL, TG

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10
Q

Renal failure

A

Increase TC, TG, decrease HDL

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11
Q

Obesity

A

Decrease HDL and TG Increases

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12
Q

Cirrhosis

A

Increase TC, TG and decrease HDL

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13
Q

High cholesterol diet

A

Increase TC, LDL, HDL remains the same

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14
Q

High SFA diet

A

Increase in TC, LDL, HDL

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15
Q

High Trans fat diet

A

Increase TC, LDL while decreasing HDL

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16
Q

High sugar diet

A

Increase TG while decreasing HDL

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17
Q

High alcohol diet

A

Increase HDL and TG

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18
Q

Smoking

A

TC and LDL increase or remain the same while HDL decreases

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19
Q

Lack of PA

A

HDL decreases while TG increases

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20
Q

Explain the effects of obesity on lipoprotein metabolism

A

Excessive dietary consumption (CHOs) and alcohol will suppress oxidation of Acyl-CoA –> Packaged into VLDL, increasing lipogenesis while lipolysis increases and TGs uptake into the peripheral tissues

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21
Q

What is the consequence of increased production of VLDL and increased lipolysis in obesity?

A

Normal VLDL and LDL, but increased fat deposits (adipose tissue). HDL will NOT decrease if this balance is achieved

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22
Q

How is hyperTG caused in obesity?

A

May have a defect in the lipolytic effect (HSL) and will cause an accumulation of VLDL (not deposited), causing hyperTG and likely decreased HDL

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23
Q

How is hypercholesterolemia caused in obesity?

A

Defective LDL receptor, high SFA diet

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24
Q

(T/F) All individuals who are obese have high LDL levels

A

FALSE, need a defective receptor, or high SFA intake

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25
Q

There is likely an increase in VLDL in obesity (due to high dietary intakes) what explain the HDL lowering relationship?

A

As VLDL increases, CETP activity will increase as more TG (from VLDL) is exchanged for a CE (from HDL). HDL that is saturate with TG will be destined for catabolism in adipose tissue and in liver

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26
Q

What is higher BMI associated with?

A

Lower HDL

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27
Q

(T/F) Higher BMI is associated with higher LDL

A

False, associate with lower HDL

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28
Q

What are the two key factors associated with low HDL?

A

High BMI

Abdominal obesity

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29
Q

(T/F) There is a stronger association with total body fat than abdominal fat in lower HDL

A

False, stronger correlation with higher abdominal fat and lower HDL levels

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30
Q

Abdominal fat and lower HDL is has a more stronger association in ___

A

Men and post-menopausal women

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31
Q

Besides uptake and catabolism in LIVERR of HDL once saturated with TG, what are other possible mechanism?

A

Increased HDL uptake by adipocytes

Increased clearance of Apo-A1

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32
Q

Which form of HDL is likely to undergo RCT? Which form is transported to liver?

A

HDL3

HDL2

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33
Q

According to the CCS 2016 guidelines, which ages should be screened for CVD risk? Ethnic groups?

A

Men AND Women > 40 y/o

High risk ethnic groups: south asian, indigenous

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34
Q

Which conditions require screening for CVD risk despite age? (A-CAD-OF)

A
  • Arterial HTN
  • Clinical evidence of atherosclerosis
  • Abdominal aortic aneurysm
  • DM
  • Obesity
  • Family history
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35
Q

What is sceened?

A
  • History and physical examination
  • Standard lipid panel
  • Glucose
  • eGFR
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36
Q

What is included in a standard lipid panel?

A

TC
LDL-C
HDL-C
TG

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37
Q

Lipid testing can be done ___

A

non-fasting

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38
Q

What is optional in-screening?

A
  • Apo-B instead of LDL cholesterol

- Urine albumin:creatinine ratio (renal function)

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39
Q

(T/f) Fasted lipid and lipoprotein testing is recommended

A

F, non-fasting (more accessible)

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40
Q

When should individuals have fasted lipid and lipoprotein testing?

A

If TG levels >4.5 mmol/L

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41
Q

In non-fasting lipid and lipoprotein levels, how will lipid panel be affected?

A
  • Minimal change in non-HDL-C
  • Slight decrease in LDL-C
  • Small increase in TG
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42
Q

What is promoted to calculate non-HDL C?

A

TC - HDL-C = non-HDL C

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43
Q

CV risk assessment to be completed every ___ for men and women aged ___

A

3-5 years

40-75

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44
Q

What are the two risk assessment models?

A 
10-year (Framingham Model)
Cardiovascular Age (CV Life Expectancy Model)
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45
Q

Whats important about the risk assessment tool?

A

Info should be shared with patients to support shared decision making and improve the likelihood that they will reach lipid-targets

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46
Q

How was the 10-year FRS developed?

A

Assessed a baseline of a population, then followed them for as long as possible and were able to track risk factors that contributed or did not contribute to their development of CVD/mortality

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47
Q

Describe the steps used in the FRS scoring model

A

1) Gender, age group, lipid-profile, BP, smoking and diabetes risk points are added.
2) Using risk points from step 1, patients 10 -year CVD risk % can be identified.
3) Using risk points calculated in Step-1, we can also determine cardiovascular age.
4) Based on the 10-year CVD risk %, we can determine if patient is low, moderate or high-risk

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48
Q

What is important concerning family history and FS score? (Modified FRS score)

A

That is 10-year risk % DOUBLES for individuals between the ages of 30 and 59 without diabetes and in presence of a positive family history of premature CVD

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49
Q

High risk FRS?

A

> /= 20%

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50
Q

Low risk FRS?

A

<10%

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51
Q

Intermediate risk FRS?

A

10-19%

52
Q

Statin indicated conditions? (CAC-D)

A
  • Clinical atherosclerosis
  • Abdominal aortic aneurysm
  • Chronic Kidney disease
  • Diabetes (most)
  • LDL-C >/= 5 mmol/L
53
Q

When is diabetes a statin indicated condition?

A
  • Age >40 y/o
  • Age > 30y y/o and 15 yr duration (T1DM)
  • Microvascular disease
54
Q

Statin indicated LDL-C level?

A

> /= 5 mmol/L

55
Q

Primary prevention conditions?

A
  • Intermediate Risk
  • FRS >/= 20%
  • Men over 50 and women over 60 with one additional risk factor
56
Q

What are intermediate risks that qualify for primary prevention conditions? (Hint FRS between 10-19% and [3])

A 
FRS 10-19% AND:
-LDL >3.5 mmol/L
OR
-Non-HDL-C > 4.3 mmol/L
OR
-Apo-B > 1.2 g/L
57
Q

What additional risk factors for men over 50 and women over 60 pose an intermediate risk that qualify for primary prevention conditions?

A
  • Low HDL-C
  • Impaired fasting glucose
  • High waist circumference
  • Smoker
  • HTN
58
Q

(T/F) Patient with High risk FRS (>/= 20%) is a statin-indicated condition

A

F, is a primary prevention condition

59
Q

(T/F) Patient with FRS of 15% and LDL-C of 4 mmol/L is a primary prevention condition

A

True

60
Q

What indicates Low risk and no Pharmacotherapy

A

FRS <10%

61
Q

What does non-HDL cholesterol include?

A

All Apo-B particles, LDL, VLDL, IDL, Lp(a), CM, CM remnants

62
Q

Apo-B containing lipoproteins are known as ____ and are ____

A

Non-HDL cholesterol, atherogenic

63
Q

What is recommended as an alternative target to LDL-C when evaluating risk in adults?

A

Non-HDL-C and Apo-B

64
Q

What must be considered when using HDL-C and Apo-B?

A

Value and preferences, as most clinicians are most familiar with LDL-C and we recommend its use as the primary target, but recognize the advantages of non-HDL-C and Apo-B

65
Q

(T/F) Stating therapy is recommended for patients with FRS <10%

A

False

66
Q

Primary target goal in high risk patients? Coronary disease?

A
  • <2 mmol/L or >50% decrease in LDL-C

- <1.8 mmol/L if coronary disease

67
Q

Primary target goal in intermediate risk patients?

A

<2 mmol/L or >50% decease in LDL-C (Same as high risk)

68
Q

Primary target goal in low risk patient?

A

> 50% decrease in LDL-C

69
Q

Alternative target goal in high risk patients?

A

-Apo-B <0.8 g/L or non-HDL <2.6 mmol/L

70
Q

Alternative target goal in intermediate risk patients?

A

Same as high risk

71
Q

Alternative target goal in low risk patients?

A

None

72
Q

Define atherosclerosis

A

Thickening of the blood vessel wall caused by the presence of an atherosclerotic plaque

73
Q

When is the ath plaque dangerous?

A

If it completely blocks off or ruptures (ischemia)

74
Q

What are the two hypothesis of the development of ath? Where do they link?

A

Endothelial injury and lipid-filtration, where oxidized LDL, macrophages and fatty streak will contribute to the endothelial injury

75
Q

Describe the endothelial injury hypothesis

A

Damage to endothelial wall, which causes the adherence of platelets which will release platelet-derived growth factors. This will encourage cell proliferation and migration, eventually resulting in the formation of a lesion

76
Q

Describe the lipid-infiltration process

A

High amounts of circulated LDL will enter sub-endothelial space, will become oxidized, engulfed by macrophages to become foam cells and result in the formation of a fatty streak.

77
Q

Damage to endothelial wall?

A
  • HTN
  • Smoking
  • Ang II
  • Decreased NO (Smoking, Ang II)
  • Glycated proteins
  • Oxidized LDL
78
Q

Explain the progression of ath to foam cells.

A

LDL exceeds endocytic capacity, and infiltrates into sub-endothelial space. Subject to oxidation, monocytes transmigrate the endothelium and become macrophages and engulf the oxidized LDL, becoming foam cell.s

79
Q

What cytokines do macrophages secrete? Which one interacts with CRP (from liver) to activate other inflammatory molecules?

A
  • TNF-alpha
  • IL-G –> Interacts with CRP
  • IL-1
  • NF-xB
80
Q

Macrophages secrete cytokines, what else does it activates? What does that secrete?

A

T-cell
-TNF-alpha
-IFN-gamma
Further aggravates the inflammatory state

81
Q

Explain the formation of the fibrous cab

A

Endothelial cells will secrete growth factor FGF and FDGF which will promote smooth muscle cell migration and proliferation. Smooth muscle cells secrete collage –> Formation of the fibrous cap. Accumulation of these cells contributes to the narrowing of the vessel.

82
Q

What is a smooth muscle derived foam cell? How is it sustained?

A

When the fibrous cap attracts lipids, will be sustained by the growth of a blood vessel.

83
Q

Examples of ath risk factors

A
  • Family history
  • Age/Sex (65 y/o W and 55 y/o M)
  • Obesity (abdominal)
  • Dyslipidemia
  • HTN
  • DM
84
Q

(T/F) Hyperlipidemia is always a risk factor for atherosclerosis

A

FALSE - hyperlipidemia also includes high HDL, which would be a good thing

85
Q

Irreversible RF CVD?

A
  • Age
  • Male
  • Genetics
86
Q

Age CVD increases men?

A

Men over 55

87
Q

Age CVD increased women?

A

Women over 65

88
Q

Reversible RF CVD?

A
  • DM
  • HTN
  • Abdominal obesity
  • Hyperlipidemia
  • Low HDL C
89
Q

Low HDL C men?

A

<1.0 mmol/L

90
Q

Low HDL C women?

A

<1.3 mmol/L

91
Q

Apo-B 100 is of _____ origin

A

Hepatocyte

92
Q

Apo-B 48 is of ____ origin

A

Enterocyte

93
Q

Explain the endogenous pathway of cholesterol metabolism

A

Learn it

94
Q

Explain the exogenous pathway of cholesterol metabolism

A

Learn it

95
Q

CM and VLDL

A

contain more TG

96
Q

LDL contains more

A

CE

97
Q

HDL contains more

A

Apo-P and phospholipids

98
Q

Normal TC

A

<5.2 mmol/L

99
Q

Normal HDL

A

1.-1.5 mmol/L (Higher the better)

100
Q

Normal LDL

A

<2.6 mmol (High risk should aim for lower)

101
Q

Normal TG

A

<1.7 mmol/L

102
Q

Function of apoproteins?

A
  • Stability
  • Activation of enzymes (Apo-CII)
  • Interact with receptors (Apo-B100)
103
Q

Apoproteins are major determinants if what?

A

The metabolic fate of lipoproteins:

  • changes is composition
  • indicative of # in plasma
  • indicative of presence/severity of diseases
104
Q

CM apoproteins?

A

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

105
Q

VLDL apoproteins

A

B-100
C-II
E

106
Q

What is the issue is Apo-E mutations?

A

Exchangeable, and can be found on any lipoprotein where an mutation can have great effects on lipoprotein metabolism

107
Q

Most common Apo-E mutation? Most detrimental?

A

Apo E3/E3

Apo E2/E2 (least common)

108
Q

What happens in the Apo E2/E2 mutation?

A

Generates an apolipoprotein that will NOT be recognized by the LDL receptor

109
Q

Primary cause of dyslipidemias?

A

Genetics - a single or polygenetic abnormality

110
Q

Secondary cause of dyslipidemias?

A

Environments/predisposition, disease state

111
Q

What are the 3 hypolipoproteinemias? (Rare)

A

1) Abetalipoproteinemia
2) Familial hypobetalipoproteinemia
3) Familial alpha-lipoprotein deficiency (Tangiers disease)

112
Q

Abetalipoproteinemia

A

Absence in Apo-B synthesis results in no CM/VLDL/LDL and TAG accumulation in liver and intestine

113
Q

Familial hypobetalipoproteinemia

A

Decrease in apo-B synthesis results in LDL levels 10-50% of normal range while CM remains the same

114
Q

Familial alpha-lipoprotein deficiency (Tangiers disease)

A

Absence of HDL, causing CE to accumulate in tissues. Results in normal CM, VLDL, LDL but hyperTG due to lack of RCT.

115
Q

Hypercholesterolemia?

A

Increased LDL, causes vascular diseases and xanthomas. Serum remains normal. + CVD risk

116
Q

Combined hyperlipoproteinemia?

A

Mutation of LDL-receptor or apo-B. Causes increased lipid panel while HDL decreases. Symptoms include vascular diseases and serum appears lighter due to high TG. +++ CVD risk

117
Q

Hypochylomicronemia?

A

Absence or deficiency in LPL/Apo-CII - Increasing CM even during fasting and TGs while HDL decreases. . Serum is very white with band of CM on top. 0 CVD risk

118
Q

Dysbetalipoproteinemia?

A

E2/E2 not recognized, accumulation of VLDL/IDL. Serum more white and IDL accumulates on-top.

119
Q

Hypertriglyceredemia?

A

Accumulation of TG and VLDL, while HDL decreases.. Exacerbated by alcohol and diabetes. Serum white due to TG accumulation.

120
Q

Mixed hyperlipidemia ?

A

Visual band of CM floating within blood, high TG and VLDL. Serum white with CM band.

121
Q

Which serums appears normal?

A

Hypercholesterolemia, as only LDL increases

122
Q

Which serum appears white-ish?

A

All but hypercholesterolemia

123
Q

Which serum has band of CM?

A
  • Hyperchylomicronemia

- Mixed Hyperlipidemia

124
Q

Which serum has IDL band?

A

-Dysbetalipoproteinemia

125
Q

Explain why obesity is not a major risk factor for dyslipidemia’s?

A

Obesity primarily only lowers HDL as TG is elevated. Co-morbidities associated with obesity are more likely to pose risk factors.

126
Q

What is the effect of obesity on dyslipidemia?

A

Constant flux of FFA during fed and fasted state. In fasted state, HSL activity is increased (likely due to insulin resistance)

Clinical Nutrition 1 (30 decks)

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