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Clinical Nutrition 1 > Dyslipidemia & CVD 1 > Flashcards

Dyslipidemia & CVD 1 Flashcards

1
Q

Guidelines to consult for dyslipidemia in Canada

A

The Canadian cardiovascular Society’s Dyslipidemia Guidelines

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2
Q

Trend of mortality from CVD in past decade

A

40% decrease in mortality from CVD

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3
Q

Why decrease in mortality from CVD

A
  • improvement in control of CVD risk factors

- medical management of patients with CVD

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4
Q

2nd cause of death

A

CVD (1st= cancer)

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5
Q

Role of cardiovascular system

A
  • regulates blood flow to tissues
  • thermoregulation
  • hormone transport
  • maintenance of fluid volume
  • regulation of pH
  • gas exchange
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6
Q

How the cv system regulates blood flow to tisses

A
  • delivers oxygenated blood and nutrients

- retrieves waste products

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7
Q

Major forms of cardiovascular disease

A
  • hypertension
  • atherosclerosis
  • coronary heart disease
  • peripheral vascular disease (cerebrovascular disease; deep vein thrombosis)
  • congestive heart failure
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8
Q

Atherosclerosis =

A

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

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9
Q

Atherosclerosis results in :

A

restriction of arterial blood flow (due to the plaque)

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10
Q

Atherosclerosis is associated with :

A
  • myocardial infarction (MI°
  • cerebrovascular accident (CVA or stroke)
  • peripheral vascular disease (PVD)
  • coronary heart disease (CHD)
  • congestive heart failure (CHF) when severe CHD or MI occurs
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11
Q

Cells involved in atherosclerosis

A
  • endothelial cells
  • smooth muscle cells
  • platelets
  • leukocytes
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12
Q

How atherosclerosis begins

A

Begins as a response to endothelial lining injury that results in an inflammatory process

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13
Q

Symptoms of atherosclerosis

A

asymptomatic until it progresses to ischemic heart disease

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14
Q

3 steps of formation of atherosclerotic plaque

A

1) Injury of endothelial wall, monocytes respond to injury and infiltration under the lining
2) Monocytes slip under blood vessel cells and engulf LDL cholesterol, becoming foam cells. Fatty streaks develop.
3) fatty streak thickens and forms plaque as it accumulates additional lipids, smooth muscle, CT, cellular debris

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15
Q

Key cells that react to endothelial injury

A

monocytes = phagocytic WBC

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16
Q

What are fatty streaks

A

the thin layer of foam cells that develop on artery walls

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17
Q

Primary causes of endothelial wall damage

A
  • high blood pressure
  • chemicals from tobacco
  • oxidized LDL
  • glycated proteins
  • low nitric oxide
  • angiotensin2
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18
Q

In which disease would you have glycated proteins

A

Uncontrolled diabetes leads to chronic hyperglycaemia in circulation

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19
Q

Consequence of decreased nitric oxide

A

vasoconstriction

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20
Q

2 hypothesis that used to describe the atherogenesis (discovered they are linked)

A
  1. Endothelial-Injury hypothesis

2. Lipid-infiltration hypothesis

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21
Q

Endothelial-Injury hypothesis

A

endothelial injury -> adherence of platelets -> release of platelet-derived growth factor-> cell proliferation -> advanced lesion (atheroma)

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22
Q

Lipid-infiltration hypothesis

A

high plasma LDL level -> LDL infiltration into intima -> oxidised LDL plus macrophages -> foam cells -> fatty streak

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23
Q

How are the 2 theories linked?

A

Oxidized LDL + macrophages and fatty streak both cause endothelial injury

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24
Q

T/F

High LDL causes foam cells and thus atherosclerosis

A

F

Need an injury to contribute to atherosclerosis

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25
Q

Biomarker of atherosclerosis

A

CRP

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26
Q

Risk factors for developing atherosclerosis

A
  • family history
  • age and sex (more in men, 65+)
  • obesity (+ly associated with dyslipidemia, HTN, physical inactivity, diabetes)
  • dyslipidemia
  • hypertension
  • physical inactivity
  • diabetes mellitus
  • impaired fasting glucose/metabolic syndrome
  • cigarette smoke
  • obstructive sleep apnea
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27
Q

Typical patient at high risk for atherosclerosis

A
  • man
  • 65+
  • obese
  • smokes
  • physically inactive
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28
Q

Atherosclerosis less prevalent in women, why

A

Because estrogen is protective against atherosclerosis (post menopausal women have a risk similar to men)

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29
Q

Which risk factor for atherosclerosis can be revered?

A

Physical inactivity

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30
Q

How can hypertension be a risk for developing atherosclerosis

A
  • may initiate an atherosclerotic lesion

- can cause plaque to rupture

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31
Q

Chylomicrons

A

lipoproteins formed by intestine after we ingest a meal with fat, are carriers of ingested TG

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32
Q

Enzyme that lines blood vessels and hydrolyses TG

A

Lipoprotein lipase

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33
Q

Apoprotein on VLDL

A

ApoB-100 (from liver)
Apo E
Apo C

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34
Q

Apoprotein on CM

A 
Apo B-48 (from intestine)
Apo A-I
Apo A-IV
Apo C-II
Apo C-III
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35
Q

Apoprotein on HDL

A

Apo A-1
Apo A-II
Apo C
Apo E

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36
Q

Lipoprotein with the most TG

A

CM

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37
Q

Lipoprotein with the least TG

A

HDL

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38
Q

Lipoprotein with the most cholesterol esters

39
Q

Lipoprotein with the most ApoP

40
Q

Desirable range for total cholesterol

A

< 5.2 mmol/L

41
Q

Normal HDL range

A

1.0 - 1.5 mmol/L
>1.0 men
>1.3 women

42
Q

Optimal LDL range

A

< 2.6 mmol/L (but already is low)

43
Q

Optimal TG range

A

< 1.7 mmol/L

44
Q

Apoprotein Functions

A
  • synthesis/secretion of specific lipoproteins
  • stabilize coat of lipoprotein
  • activate enzymes
  • interact with cell surface receptors
45
Q

apoC-II activates

46
Q

LDL receptors react with which apoprotein

47
Q

Apoproteins reflect

A
  • changes in lipoprotein composition

- indicative of number of lipoproteins in plasma

48
Q

Apoproteins used to diagnose what?

A

In diagnostic of lipoprotein disorders and risk for developing CHD or CVD

49
Q

Apoproteins are predictors of what?

A

May be better predictors of heart disease than lipid levels and may correlate with the severity of the disease

50
Q

Most common ApoE genotype (60% frequency)

A

E-3/E-3

carrier of double allele

51
Q

Least common ApoE genotype (1% frequency)

52
Q

What is unusual of Apo E-2/E-2

A

Does not bind to LDL receptors –> high VLDL remnants –> risk of dyslipidema

53
Q

Primary (or Familial) dyslipidemia classification

A

Single or poly-genetic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia

54
Q

Secondary dyslipidemia classification

A
  • environmental causes +/- predisposition
  • happens later in life
  • more prevalent
  • due to other causes than genetic
55
Q

How to diagnose primary dyslipidemia

A
  • history (age at onset, family members)
  • physical signs
  • lab analysis
  • appearance of serum
  • genetic sequencing for rare cases
56
Q

Physical signs of 1° dyslipidema

57
Q

Lab analysis of 1° dyslipidema

A

lipid profile, apoproteins, LPL activity

58
Q

Serum of 1° dyslipidemia

A

Appears white

59
Q

2 types of Familial Dyslipidemias

A
  • hypolipoproteinemia (rare

- hyperlipoproteinemias (common)

60
Q

3 types of hypolipoproteinemia

A
  • Abetalipoproteinemia
  • Familial hypobetalipoproteinemia
  • Familial alpha-lipoprotein deficiency (Tangier disease)
61
Q

Abetalipoproteinemia

A
  • Defect in apoprotein B synthesis
  • No chylo, VLDl, LDL formed
  • TAG accumulate in liver and intestine
62
Q

Familial hypobetalipoproteinemia

A

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

63
Q

Familial alpha-lipoprotein deficiency

A
  • Virtual absence of HDL (Apo-AI)
  • CE accumulate in tissues
  • Chylo, VLDL, LDL are normal
  • Moderate hyper TG
64
Q

5 phenotypes of hyperlipoproteinemia

A 
I: high CM
IIa: high LDL
IIb: high LDL +VLDL
III: high beta VLDL
IV: high VLDL
V: high Chylo + VLDL
65
Q

Most prevalent phenotype

A

IV and IIB

66
Q

Xanthomas are a symptom of which type of hyperlipoproteinemia

A

Type III

dysbetalipoproteinemia

67
Q

Out of VLDL, LDL, TG which is he most atherogenic?

68
Q

Are xanthomas reversible?

69
Q

Lifestyle factors that cause secondary dyslipidemia

A

Diet (high: cholesterol, saturated fats, trans fats, sugars)
Alcohol
Smoking
Lack of physical activity

70
Q

High cholesterol increase:

A
  • Total cholesterol
  • LDL-C

(HDL-C stays the same)

71
Q

High saturated fats increase:

A
  • Total cholesterol
  • LDL-C
  • HDL-C
72
Q

High trans fats increase, decrease:

A

Increase:

  • Total chol
  • LDL-C

Decrease:
-HDL-C

73
Q

Alcohol increases:

A
  • HDL-C

- TG

74
Q

Lack of physical activity increases, decreases:

A

Increase:
-TG
Decrease:
-HDL-C

75
Q

Diseases that cause secondary dyslipidemia are

A 
diabetes
hypothyroidism
renal failure
obesity
cholestasis
chirrhosis
myelomas
Cushing syndrom
76
Q

Medication that cause secondary dyslipidemia are:

A 
thiazide diuretics
beta-blockers
corticosteroids
estrogens
progesterone
benzodiazepine
retinoic acid
antiretroviral
77
Q

Obesity effects on lipoprotein metabolism

A

Increased substrate flux to liver
Can be :
-Postprandial = due to excess kcal (lipids, carbs)
-Postabsorptive = due to high adipose tissue and hormone-sensitive lipase activity resulting in increased FFA flux to liver

78
Q

Why is hormone-sensitive lipase activity high in obese

A

because of insulin resistance

79
Q

What is associated with low HDL-C

A
  • high BMI

- abdominal obesity

80
Q

Association between abdominal/visceral fat and HDL

A
  • strong association with HDL

- strong association in men and post-menopausal women

81
Q

Relationship between BMI and HDL

A

Inverse linear relationship

- stronger association of BMI with HDL than LDL

82
Q

Mechanisms associated with reduced HDL-C in obesity

A
  • association with hyperTG (high VLDL -> high CETP -> high hepatic lipase -> liver uptake)
  • increased uptake of HDL2 by adipocytes
  • increased clearance of apoA1 –> HDL catabolism
83
Q

Who should be screened for CVD?

A
  • Men 40+

- Women 40+ (OR postmenopausal)

84
Q

Patients with which conditions should be screened regardless of age?

A
  • Clinical evidence of atherosclerosis
  • Abdominal aortic aneurysm
  • Diabetes mellitus
  • Arterial HTN
  • Cigarette smoking
  • Clinical signs of dyslipidemia
  • Family history of dyslipidemia or premature CVD
  • Chronic kidney disease
  • Obesity
  • HIV infection
  • Inflammatory disease
85
Q

How to screen for all

A
  • history and physical examination
  • standard lipid panel
  • nonHDLC
  • glucose
  • eGFR

optional:
- ApoB
- urine albumin:creatinine ratio

86
Q

Is fasting required for lipid testing ?

87
Q

2016 recommendations for a CV risk assessment ?

A
  • Every 3-5 years for men and women age 40-75

- OR when risk status changes

88
Q

Framingham risk score

A

= estimation of 10-year cardiovascular disease risk

89
Q

Important risk factors the FRS uses

A
  • Sex
  • Age
  • HDL chol
  • Total chol
  • Blood pressure
  • Diabetes
  • Smoking
90
Q

Important risk factors the FRS uses to predict CVD

A
  • Sex
  • Age
  • HDL chol
  • Total chol
  • Blood pressure
  • Diabetes
  • Smoking
91
Q

Why are TG not part of risk assessment

A

they are not very atherogenic

92
Q

How to interpret the FRS

A

3 risk levels:

  • High (20%+)
  • Intermediate (10-19%)
  • Low (10%-)
93
Q

Statin should be prescribed in which cases

A
  • clinical atherosclerosis
  • abdominal aortic aneurysm
  • LDL-C > 5mmol/L
    -chronic kidney disease
  • diabetes IF
    age 40+ OR
    age 30+ and 15y duration OR
    Microvascular disease

Clinical Nutrition 1 (13 decks)

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