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Clinical Nutrition 1 > Dyslipidemia Part II > Flashcards

Dyslipidemia Part II Flashcards

1
Q

Global lifestyle modification approach?

A
  • Diet

- Weight management

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2
Q

Why is weight management indirect cause of dyslipidemia?

A

Will serve to lower HDL levels, not our number one priority

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3
Q

Weight loss can cause __

A

Decreased LDL, HDL and TG. After maintenance, HDL will increase

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4
Q

PA of 1200-2200 kcal/week on lipids?

A

Decease TG and LDL while increasing HDL .. compares to the effects of medication.

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5
Q

________ exercise has the greatest benefits while ____ has little effect

A

Volume/Intensity

Resistance

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6
Q

Who set the stage that dietary cholesterol increases cholesterol in circulation?

A

Ancel-keys

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7
Q

What did the predictive equation show?

A

The constant relating to the change in sat fat is higher than the change inc cholesterol and PUFA

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8
Q

Limitations of predictive equations?

A
  • Not all sat fats the same
  • We now measure lipid fractions (measures total cholesterol)
  • Assumes MUFA and CHO are neutral
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9
Q

Key point from Ancel-Keys 7 country study?

A

High cholesterol increases with mortality, EXCEPT for Crete - med diet and protective effects.

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10
Q

(T/F) Everyone responds to dietary cholesterol

A

False

Compensators (2/3) vs. non-compensators (1/3)

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11
Q

______ decease in dietary cholesterol results in 0.05-0.2 mmol/L decrease in TC

A

100 mg/day (not huge)

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12
Q

How does increased blood cholesterol impact LDL receptors?

A

Reduce activity of receptors in the liver, and the cholesterol in storage will decrease synthesis and will inhibit any further uptake from bloodstream –> Cholesterol remains in the bloodstream,

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13
Q

What are other effects of high blood cholesterol?

A
  • Increase CM and remnants
  • Increase VLDL
  • Interferes with ability of HDL to clear cholesterol
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14
Q

(T/F) Cholesterol always linked with fat content

A

False, such as in seafood

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15
Q

Why should we NOT limit fat?

A

Because if we sub with simple CHO, will increase TG and decrease HDL

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16
Q

Recommended vs. current intake of fat?

A

25-35%
34-27%
We need to focus on QUALITY

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17
Q

What may decrease HDL?

A

Very low fat diets

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18
Q

What is the effects of SFA?

A
  • Decrease clearance of VLDL and LDL
  • Reduce LDL receptor activity
  • Reduce transcription
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19
Q

How does SFA interact with phospholipids?

A

Alter PL composition of cell membrane and influence activity and binding by changing the lipoprotein surface

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20
Q

Goal of SFA?

A

<10% calories

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21
Q

Issue in NA and SFA?

A

Consuming LARGE amounts of foods than contain moderate amounts of SFA (processed foods)

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22
Q

What is the controversy with SFA?

A

Will increase HDL alongside LDL, and clear link between SFA and CVD is not clear

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23
Q

Replacing SFA with MUFA PUFA =

A

Improve lipid profile and CVD risk

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24
Q

What is the recommendation in Canada on SFA?

A

Currently no limit, but instead focus on healthy balanced diet, more MUFA and PUFA and less processed sources of SF

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25
Q

MC SFA

A

Caprylic and Caproic

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26
Q

IC SFA

A

Lauric

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27
Q

LC SFA

A
  • Myrstic
  • Palmitic
  • Stearic
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28
Q

Carylic/Caproic?

A

No effects on scerum cholesterol

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29
Q

Lauric?

A

Increase LDL and HDL

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30
Q

Myristic?

A

Incease LDL

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31
Q

Palmitic?

A

Increase LDL, but usually only in presence of high dietary cholesterol

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32
Q

Stearic?

A

Neutral effect compared to other SFAs

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33
Q

Which SFA increase LDL? (LMP)

A

Lauric
Myristic
Palmitic

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34
Q

MCT <10 have ____

A

no effects on serum cholesterol

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35
Q

SFA have no effect on ___

A

VLDL

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36
Q

How does SFA from dairy products pose a neutral CVD risk?

A

Raise LDL but augment size of particles - and less atherogenic

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37
Q

_____ of cheese does not have the negative impact on CVD risk such as butter

A

Physical matrix

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38
Q

Coconut oil is mostly ____ which increases LDL and HDL

A

Lauric

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39
Q

(T/F) Chicken fat is mostly SFA

A

False, is mostly PUFA (not all animal fats are SFA)

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40
Q

Oleic acid –>

A

Eicosatrienoic acid

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41
Q

Linoleic acid (omega 6) –>

A

Arachidonic acid

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42
Q

Linolenic acid (omega 3) –>

A

Docosahexanoic acid

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43
Q

When we replace SFA in the diet with PUFA, such as omega-6. The LDL-lowering effect is partly passive, why?

A

Omega-6 will increase LDL clearance by suppressing the effects of SFA

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44
Q

When can omega-6 negatively impact lipid profile?

A

A diet very rich in PUFa may decrease HDL and apo-AI especially if >10% of total kcal.

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45
Q

What may a high PUFA diet do?Why?

A
  • Increase inflammation and increased oxidative damage to LDL
  • Double bond formation of PUFA means it is more susceptible to oxidation
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46
Q

PUFA goal %?

A

Goal is 5-10% of calories

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47
Q

MUFA % goal?

A

No more than 20% total calories

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48
Q

Compared to PUFA, MUFA does not ____ and is beneficial when substituted from ___

A

lower HDL

SFA

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49
Q

Advantages of MUFA (4)

A
  • Do not decrease HDL
  • Less oxidation
  • Do not increase TG
  • Do not increase cancer
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50
Q

Dietary sources of linoleic acid

A
  • Safflower oil
  • Sunflower oil
  • Soybean oil
  • Corn oil
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51
Q

Dietary sources of oleic acid

A
  • Olive oil
  • Canola oil
  • Peanut oil
  • Nuts
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52
Q

What are the two animal sources of Omega-3?

A

EPA: Eicopentanoic acid
DHA: Docahexanoic acid

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53
Q

What is the plant source of omega-3?

A

Alpha-linolenic acid

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54
Q

Omega-3s do what in hyperlipidemic patients?

A

Decrease TG

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55
Q

There is an inhibition of ____ associated with consumption of Omega-3

A

VLDL-TG

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56
Q

(T/F) Omega-3s decrease LDL

A

False, they decrease content of TGs synthesis within the VLDL particle

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57
Q

What is the key role of Omega-3 and decreasing CVD risk?

A

Reducing platelet aggregation and prevent coronary thrombosis, retard the proliferation of fibroblasts

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58
Q

(T/F) Evidence is strong enough in omega-3 and CVD risk to recommend supplements

A

F

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59
Q

How do omega-3s impact the progression of atherosclerosis?

A

By preventing the inflammation that occurs in atherosclerosis

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60
Q

How do trans-fats render LDL more atherogenic?

A

By increasing number and decreasing size

61
Q

What are the other disadvantages of trans-fats?

A
  • Reduce HDL

- Increase inflammatory markers and endothelial damage

62
Q

Goal for fibre? From grains/cereals?

A

20-30 g/day where 50% should be soluble (cereals and grains)

63
Q

What does soluble fibre decrease?

A

Total C and LDL-C

64
Q

What is another benefit of fibre?

A

Lower energy and fat intake

65
Q

Overconsumption of simple carbs will increase __ and decrease

A

VLDL-TG

HDL-C (as TG are increased)

66
Q

What will overproduce VLDL-TG without excess/overconsumption?

A

ANY consumption of high fructose corn syrup

67
Q

How does excess carbs result in more TGs?

A

Lead to accumulation of Acyl-Coa (Glycogen limit exceeded) and will be destined for TG synthesis.

68
Q

Does fructose in fruits cause same effect as HFCS?

A

NO -due to small amounts

69
Q

Disadvantages of high CHO diet?

A
  • Decreased HDL and increased TG
  • HyperTF
  • May increase blood glucose and hyperinsulinemia
70
Q

What may elevate HDL and inhibit cell-mediated oxidation of lipoproteins?

71
Q

Which polyphenol is found in alcohol?

A

Reveratrol

72
Q

(T/F) Consumption of alcohol is recommended especially for those with established CHD

73
Q

What does alcohol inhibit? When should it be avoided?

A

Acyl-CoA –> TG

Avoid in hypertriglyceridemia

74
Q

Effects of soy-protein?

A

Reduction in TC, LDL-C and TG without an effect on HDL-C in patients with or without CVD

75
Q

What is found in soy protein?

A

Isoflavones and phytoestrogens

76
Q

What is the US and Canada Health claim about soy protein ?

A

25 grams of soy protein as part of a diet low in cholesterol and saturated fat may reduce the risk of heart disease

77
Q

How do antioxidants reduce atherosclerosis risk?

A

Inhibit LDL-ocidtion

78
Q

Should we supplement with antioxidants?

A

No firm recommendations - focus on varied diet

79
Q

When do levels of homocysteine increase risk of heart disease?

A

If greater than 14 umol/L

80
Q

Each increase of _____ of fasting concentration of homocysteine will increase CVD by ____

A

5 umol/L

1.6-1.8 fold

81
Q

Elevated homocysteine levels appear in up to ___ of patients with CVD

82
Q

When are folate supplements recommended?

A

In persons with high levels of hct or family history of CVD

83
Q

(T/F) Low levels of B12 are associated with an increased risk of CHD

A

False, low levels of folate are. B12 has not been associated

84
Q

Phtyosterols and stanols are plant cholesterols which will compete with cholesterol absorption, and increasing fecal excretion. What is the main source?

A

Fortified margarines (hard to obtain recommended amount in natural foods)

85
Q

Nuts are rich in what? Which nut is rich in SFA?

A
  • MUFA, PUFA

- Brazil nuts

86
Q

What else are nuts rich in?

A
  • Protein
  • Soluble fibre
  • Folic acid
  • Antioxidants (NO precursor)
87
Q

_____ of nuts reduced risk of CHD and moderate intake improves ___

A

High intake

endothelial function

88
Q

(T/F) There is a signifiant impact of nuts on body weight

89
Q

What is the FIRST target in the dietary approach for dyslipidemia?

A

Lowering LDL-C

90
Q

What is the TLC model?

A

Therapeutic Lifestyle changes

91
Q

What does TLC recommend in terms of SFA and cholesterol for those who are at higher risk?

A

<7% SFA and <300 mg cholesterol

92
Q

SFA recommendations?

93
Q

Trans fat ?

94
Q

PUFA?

A

Increase omega-3s form fish

95
Q

MUFA?

A

Use MUFA and PIUFA to replace SFA

96
Q

Cholesterol?

A

<200 mg/day for those with dyslipidemia and at high risk

97
Q

Total lipids?

98
Q

CHO?

A

Reduce simple and refined, choose whole grains

99
Q

Fibres total and soluble fibres?

A

Increase F&V and 10-25 g/day

100
Q

Protein?

A

Increase soy protein and nuts to replace animal protein

101
Q

Sterols?

A

Increase intake

102
Q

What were the results of the Med diet in the PREDIMED trial?

A

30% decrease in CV events., decreased LDL, apo-B and TG while HDL increases

103
Q

Secondary prevention is what?

A

Preventing CVD after CVD events

104
Q

What did the Lyon study find regarding the medi diet and secondary prevention?

A

70% mortality post-MI

105
Q

Describe the portfolio diet

A

Low in SFA
High in phytosterols, soy protein, soluble fiber, almonds
Vegetarian

106
Q

How much LDL decrease on portfolio diet compared to low-fat diet + statins?

A

Portfolio: 29%

Low-fat + statin: 31%

107
Q

What else decreased in the portfolio diet?

108
Q

What is a disadvantage of the portfolio diet?

A

Adherence is low (~40-45%)

109
Q

What dietary factors increases HDL?

A
  • SFA
  • Dietary choleserol
  • Alchohol (<2 drinks faily)
110
Q

What non-dietary factors increase HDL?

A
  • Long term aerobic exercise
  • Estrogen
  • Female sex
111
Q

What dietary factors decrease HDL?

A
  • Simple sugars/high-carb diet
  • PYFA
  • Obesity
112
Q

What non-dietary factors decrease HDL?

A
  • Androgens
  • Male sex
  • Anabolic steroids
  • Anti-HTN drugs
  • DM
  • Cigarettes
113
Q

First line of medicatins?

114
Q

BAS?

A

Block the enterohepatic reabsorption of cholesterol, increase excretion and may increase LDL receptors

115
Q

PCSK9 inhibitors?

A

Monoclonal antibodies block PSCK9 (enzyme), which will prevent the catabolism of the LDL-receptor which typically undergoes endocytosis and is degraded.

116
Q

Fibrates and Nicotinic acid?

A

Will aim on lowering TG in bloodstream by inhibiting VLDL production while enhancing LPL activity (more TG to tissues, less to blood)

117
Q

Effects of statin?

A

-Decreased LDL and TG while HDL increase

118
Q

Cholesterol absorption inhibitor examples?

A

-Ezetimibe

119
Q

BAS examples?

A
  • Cholestryamine

- Colestipol

120
Q

CAI effects

A

Decrease LDL

121
Q

BAS effect?

A

Decrease LDL

122
Q

PCSK9 examples?

A

Evolucumab

Alirocumab

123
Q

PCSK9 effects?

A

+++ decreased LDL

124
Q

Fibrate examples?

A

Gemfibroil

Fenofibrate

125
Q

Fibrate and nicotinic acid effects?

A

Decrease TG and LDL (more TG) while increasing HDL

126
Q

Nicotinic acid examples?

A

Nicotinic acid slow release

127
Q

Besides decreasing the endogenous synthesis of cholesterol, what else do statins do?

A
  • Decrease VLDL production, less remnants, less LDL
  • Enhances clearance of VLDL remnant and LDL
  • Increased activity of LDL receptors
128
Q

What are the adverse effects of statins?

A

-Myalgia, myopathy, increased liver enzymes, low risk of diabetes

129
Q

Which statin negatively interacts with grapefruit?

A

Simvastatin

130
Q

What is the first step to prevent non-statin add-on therapy

A

Maximize behavioural modifications and statin dose

131
Q

What can be suggested to add on if targets not yet met?

A

Ezetimibe/BAS as first line, then PCSK9 as second line

132
Q

Side effects of ezetimibe?

A

GI problems, diarrhea, rash, fatigue, muscle weakness and pain

133
Q

What may increase VLDL-C and VLDL-TG transiently, and decrease absorption of fat and liposoluble vitamins?

A

BAS (Cholestryamine)

134
Q

Side effects of BAS?

A

Significant constipation

135
Q

Side effects of PCSK(?

A

Diarrhea, muscle and joint pain

136
Q

Target TG level for high risk?

A

None, but usually should be <2.6 mmol/L

137
Q

What are the interventions for hyperTG?

A

Health behaviour interventions, then fibrates may be recommended in pateitns with extreme hyper TG (>10mmol/L)

138
Q

____ may pose No risk depending on genetic type

139
Q

When are fibrates used?

A

Highly elevated TG (Familial TG)

140
Q

Fibrate side effects?

A

Gi reactions, taste changes. abdominal pain

141
Q

Fibrate contraindications?

A

Hepatic/renal dysfunction, gallbladder disease, do NOT combine with simvastatin

142
Q

What drug is used for hypercholesterolemia, hypertriglyceridemia and hypoalphalipoproteneima?

A

Nicotinic acid

143
Q

Which drugs are NOT recommended to add-on to statin therapy?

A

Nicotinic acid and fibrates

144
Q

What is the issue with nicotinic acid?

A

Only 50-60% can tolerate, GI distress, skin flushing, itching, hepatotoxicity, arrhythmia

145
Q

What may nicotinic elevate?

A

Liver ALT and blood glucose levels

146
Q

What may be recommended to reduce side effects of nicotinic acid?

A
  • ASA to reduce flushing
  • Extended release
  • Monitor uric acid levels
147
Q

What may cause reversible increases in plasm creatinine?

148
Q

When must renal function and lipid parameters be monitored?

149
Q

In combination with statin therapy, which drugs saw further reduction on CVD events?

Clinical Nutrition 1 (30 decks)

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