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NUTR 344: Clinical Nutrition 1 > 10. Dyslipidemia and CVD 1 > Flashcards

10. Dyslipidemia and CVD 1 Flashcards

1
Q

Roles of the cardiovascular system include:

A
  • blood flow regulation to tissues (delivery of oxy-blood and nutrients; retrieval of waste)
  • thermoregulation
  • hormone transport
  • maintenance of fluid volume
  • regulation of pH
  • gas exchange
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2
Q

What are major forms of CVD?

A
  • HTN
  • atherosclerosis
  • CHD
  • peripheral vascular disease
  • CHF
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3
Q

What diseases/health issues are part of peripheral vascular disease?

A
  • cerebrovascular disease (stroke)
  • deep vein thrombosis
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4
Q

What is atherosclerosis?

What does it result in?

What is it associated with?

A
  • thickening of blood vessel walls due to atherosclerotic plaque
  • results in restriction of blood flow

Associated with:

  • myocardial infarction (MI)
  • cerebrovascular accident (CVA)
  • CHD
  • PVD
  • CHF (when severe CHD or MI)
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5
Q

How is atherosclerosis believed to develop?

What are the potential risks of atherosclerosis?

A
  • begins as inflammatory response to endothelial lining injury
  • monocytes slip inside lining, continue to engulf LDL-C and create foam cells
  • foam cells accumulate to fatty streaks that thicken with lipids, smooth muscle cells, connective tissue and debris
  • results in restriction of arterial blood flow

Risks:

  • rupture and thrombosis
  • ischemic heart disease
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6
Q

What are potential primary causes believed to lead to atherosclerosis? What is the common factor between all the theories?

A

Common factor: damage to endothelial wall

Potential causes:

  • high BP
  • tobacco chemicals
  • oxidize LDL
  • lower [NO]
  • increased angiotensin II (also contributes to lowering NO)
  • glycated proteins (linked to elevated glucose from diabetes)
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7
Q

What are risk factors for atherosclerosis?

A
  • Family history (predisposed genes)
  • Age and sex (>65y.o., males)
  • Obesity
  • dyslipidemia
  • HTN (initiate lesion or cause rupture)
  • physical inactivity
  • diabetes mellitus
  • impaired fasting glucose/metabolic syndrome
  • cigarette smoke
  • obstructive sleep apnea (hypoxia)
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8
Q

What major risk factors for atherosclerosis are reversible?

A
  • atherogenic diet
  • smoking
  • lack of physical activity
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9
Q

What major risk factors of atherosclerosis can be reversible in some cases?

A
  • diabetes
  • HTN
  • abdominal obesity
  • hyperlipidemia (LDL-C)
  • low HDL-C (men: <1.0 mmol/L, women: <1.3 mmol/L)
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10
Q

When are genetic traits and family history of CVD non-reversible risk factors for atherosclerosis?

A

When the CVD affected a primary relative under the ages of 55 (men) or 65 (women)

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11
Q

How is most cholesterol excreted?

A

Via feces

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12
Q

Concerning plasma lipoproteins in humans, what main characteristic individualizes the following lipoproteins?

  • chylomicrons
  • VLDL
  • LDL
  • HDL
A
  • Chylomicrons: highest number of core TG
  • VLDL: high number of core TG
  • LDL: highest number of core CE
  • HDL: highest number of surface Apoproteins and phospholipids
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13
Q

What are the normal levels of serum lipids?

  • Total cholesterol
  • HDL cholesterol
  • LDL cholesterol
  • TG
A
  • Tot. cholesterol: <5.2 mmol/L
  • HDL: 1.0-1.5 mml/L (>1.0 men, >1.3 women)
  • LDL: <2.6 mmol/L
  • TG: <1.7 mmol/L
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14
Q

When are LDL measurements invalid?

A

If TG levels are > 4.5 mmol/L

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15
Q

What are the main drivers of the stimulation of lipoprotein production?

A

Apoproteins

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16
Q

What are the functions of apoproteins?

A
  • synthesis/secretion of specific lipoproteins
  • stabilized surface coat of lipoproteins
  • activate enzymes
  • interact with cell surface receptors
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17
Q

What compounds are described below?

  • primary determinant of metabolic fate of lipoproteins
  • reflect changes in lipoprotein composition
  • indicative of [lipoproteins] in plasma
  • may be better predictors of heart disease (and correlate with severity)
  • help in diagnostic of lipoprotein disorders + risk for developing CHD or CVD
A

Apoproteins

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18
Q

What are the major apoproteins for each class of lipoprotein?

A
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19
Q

There are 4 different alleles for Apo-E. Which genotypes are the most frequent (bind better with LDL receptors)? Which genotypes have the lowest frequency (don’t bind to LDL receptors)?

A
  • E-3/E-3 (60%)
  • E-2/E-2 (1%)
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20
Q

What is primary dyslipidemia?

Is it common?

A
  • single or polygenic abnormalities affecting lipoprotein function resulting in hypo- or hyper-lipidemia
  • No, it is rare
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21
Q

What is a dyslipidemia diagnosis based on?

A
  • history
  • physical signs ( ex: xanthomas, …)
  • lab analysis (levels of lipids, apoproteins, LPL activity…)
  • appearance of serum
  • genetic sequencing (rare)
22
Q

Secondary dyslipidemia is caused by environmental causes and potentially predisposition to the condition. Is this a rare or common condition?

A

Common

23
Q

Hypolipoproteinemia is a rare form of primary dyslipidemia. Describe the following conditions.

  • Abetalipoproteinemia
  • Familial hypobetalipoproteinemia
  • Familial alpha-lipoprotein deficiency (Tangier disease)
A
  • Abetalipoproteinemia: defect in Apo-B synthesis, no chylo, VLDL or LDL formed, accumulation of TAG in liver/intestine
  • Familial hypobetalipoproteinemia: some Apo-B synthesis, [LDL]=10-50% of usual levels, chylo forming occurs
  • Familial alpha-lipoprotein deficiency (Tangier disease): absence of Apo-AI (HDL), CE accumulates in tissues, moderate hyperTG, chylo/LDL/VLDL normal
24
Q

Hyperlipoproteinemia is more common than hypolipoproteinemia. What are the 5 phenotypes of this condition? Which are the most prevalent?

A

Most prevelant = IIb and IV

25
Q

As a rule of thumb, elevated TG levels usually leads to a decrease in what lipoprotein cholesterol?

A

HDL-C

26
Q

Which phenotypes of primary hyperlipoproteinemia are associated with a much higher increased risk of CVD?

Which phenotype is not associated with any increase in CVD risk?

A

Most increased risk:

  • IIb: Combined; high LDL and VLDL, high apo-B, high C, high TG
  • III: Dysbetalipoproteinemia; high LDL, VLDL, and b-VLDL IDL, high TG and C

No increased risk:

  • I: Hyperchylomicronemia; high chylo fasting, high TG
27
Q

How can you differentiate the different types of hyperlipoproteinemia?

A

Through their serum patterns

28
Q

What condition has been shown to exasperate primary dyslipidemia?

A

Secondary dyslipidemia

29
Q

What are the major lifestyle causes of secondary dyslipidemia?

A
30
Q

Moderate consumption of alcohol has been linked to increased levels of _____, while higher consumption of alcohol is linked to increased levels of ______ in the blood.

A
  • HDL-C
  • TGs
31
Q

What are diseases associated with causing secondary dyslipidemia?

A
32
Q

What are medications associated with causing secondary dyslipidemia?

A
33
Q

How does obesity affect lipoprotein metabolism?

A

Causes and increased substrate flux to the liver; due to total increased intake (CHO and fat).

Postprandial: excess calories (CHO and fats)

Postabsorptive: high adipose tissue and HSL activity (insulin resistance); increased FFA flux to liver

34
Q

What is a characteristic of obesity effects on lipoprotein metabolism?

A

Increased lipolysis

35
Q

Will all obese patients have high levels of TG? Why/why not?

A
  • No
  • LDL activity is increased and more FFAs are taken up by tissues
  • Levels of lipolysis are increased in order to stabilize TGs
36
Q

What is characteristic of hypertriglyceridemia of obesity on lipoprotein metabolism?

A

Lipolytic effect: insulin-resistance, inflammation, over production of VLDL TGs

37
Q

What is characteristic of hypercholesterolemia and obesity concerning lipoprotein metabolism?

A
  • Reduced activity of LDL receptors; accumulation of VLDL remnants and LDL
38
Q

What are possible mechanisms for HDL-C lowering in obesity?

A
  • increased transfer of CE
  • increased catabolism of HDL by excess of adipose tissue
39
Q

Which has a stronger association with HDL than total body fat?

A

Abdominal obesity (visceral fat)

40
Q

BMI has an _____ _______ with HDL. It has a ______ association with HDL than LDL.

A
  • inverse relationship
  • stronger
41
Q

Both severity and distribution of obesity are associated with _____ HDL-C.

A

low

42
Q

What mechanisms are potentially responsible for lower HDL-C in obesity?

A
  • association with hyperTG
  • higher uptake of HDL2 by adipocytes
  • higher clearance of apo-A-1 (HDL catabolism)
43
Q

The CCS 2016 Guideline for Dyslipidemia Management and Prevention of CVD in Adults recommends screening men and women over _____ years old, or all patients with what conditions?

A

over 40 years of age

Conditions:

  • atherosclerosis
  • abdominal aortic aneurysm
  • diabetes mellitus
  • HPT
  • smokers
  • family history premature CVD
  • Obesity
  • HIV (high TGs)
  • Chronic kidney disease
  • ….
44
Q

Why can lipid testing be done without fasting?

A

There is very little change in lipoprotein fractions; glucose levels will increase, but there is minimal change in non-HDL-C, a slight decrease in LDL-C, and small increase in TG.

45
Q

What are the options available for screening for CV-risk assessment?

A
  • Framingham Model
  • Cardiovascular life expectancy model
46
Q

What does the Framingham Risk Score tell the patient?

What is the overall target of this method?

What is considered being high risk, according to this method?

A
  • Estimation of 10-year CVD risk
  • Decrease overall LDL-C; ***not a risk factor!
  • Scores over 20%
47
Q

Statin-induced conditions are prescribed with meds in order to reduce LDL-C levels. What are considered statin-inducing conditions?

A
  • Clinical atherosclerosis
  • Abdominal aortic aneurysm
  • Most diabetes
  • Chronic kidney disease

General dyslipidemia: LDL-C > 5 mmol/L

48
Q

Primary prevention conditions according to the CCS 2016 guidelines are for those with intermediate or high risk FRS scores. What classifies a patient as being at intermediate risk?

A

Intermediate risk (maybe meds):

  • FRS of 10-19% AND
  • LDL-C > 3.5 mmol/L OR
  • Non-HDL-C > 4.3 mmol/L OR
  • ApoB > 1.2 g/L OR
  • Men > 50, Women > 60

With 1 additional risk factor:

  • low HDL-C, impaired fasting glucose, high waist circumference, smoker, HTN
49
Q

Primary prevention conditions according to the CCS 2016 guidelines are for those with intermediate or high risk FRS scores. What classifies a patient as being at high risk?

A

FRS score of >20 %; meds prescribed to reduce risks

50
Q

With FRS < 10%, patients are considered at ____ risk for developing CVD in 10 years. What is the recommended treatment/therapy?

A
  • Low
  • No pharmacotherapy needed; just lifestyle changes to reduce risk
51
Q

Instead of directly measuring LDL-C, how are lipoproteins measured?

A

Non-HDL-C and apoB containing particles are measured together.

NUTR 344: Clinical Nutrition 1 (15 decks)

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