Exam #1: Nutrition and Cardiovascular Disease Flashcards

1
Q

What are the causative factors of vascular disease?

A
  • HTN
  • Vascular effects of DM
  • Platelet aggregation
  • Hypercoaguable states from obesity and high dietary fat
  • Smoking
  • Insufficient regular exercise
  • DIET
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2
Q

What fats have a deleterious effect on the heart?

A

1) Saturated fat

2) Cholesterol

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3
Q

What are elements of diet that can be cardioprotective?

A
  • High fiber
  • Folate
  • Anti-oxidants
  • Vitamin K
  • Low Na+
  • High K+ and Mg++
  • Omega 3
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4
Q

Where do most fatty acids in the blood come from?

A

Diet

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5
Q

What are fatty acids used for in the body?

A
  • Important membrane components
  • Precursors for hormones and other complex lipids
  • Precursor for eicosanoids
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6
Q

How are lipids transported in the blood?

A

As lipoproteins

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7
Q

List the lipoprotein classes.

A
  • Chylomicrons & remnants
  • Low Density Lipoproteins
  • High Density Liporotein
  • Very Low Density Lipoproteins
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8
Q

What are the athrogenic lipoproteins?

A
  • Chylomicron remnants
  • LDL
  • VLDL remnants
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9
Q

What are the non-athrogenic lipoproteins?

A
  • Chylomicrons
  • HDL
  • VLDL
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10
Q

What is a triglyceride?

A

Ester w/

  • 3x fatty acids
  • Glycerol
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11
Q

What is the carbon chain length for the FAs that compose TGs?

A

Even numbers:

16, 18, and 20

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12
Q

What is the function of a chylomicron?

A

Transport fat-soluble molecules from intestine to other organs

E.g.

  • Fat-soluble vitamins
  • TGs
  • Cholesterol
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13
Q

What enzyme cleaves chylomicrons to release fat-soluble molecules?

A

Lipoprotein lipase

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14
Q

What is the function of VLDL?

A

Transport lipids from liver to muscles and other organs

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15
Q

What happens to VLDL remnants?

A

Re-circulation to the liver to make LDL cholesterol

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16
Q

What is LDL cholesterol derived from?

A

VLDL

17
Q

How is LDL cholesterol taken up by the liver?

A

Receptors on hepatocytes

18
Q

What happens to LDL receptors in a high cholesterol diet? Low cholesterol diet?

A

High= fewer receptors expressed–>more circulating LDL

Low= more receptors expressed–>less circulating LDL

19
Q

How does HDL cholesterol structurally differ from the other lipoproteins?

A
  • More protein
  • More phospholipids
  • Contains LCAT enzyme
  • Contains apoE
20
Q

What are the major functions of HDL cholesterol?

A

1) Transfer ApoC-II and apoE to chylomyicrons and VLDL
2) Take up cholesterole from LDL, VLDL, and phospholipids from VLDL
3) REVERSE TRANSPORT of CHOLESTEROL

21
Q

What are the bad dietary fats?

A

Saturated fats:

  • Myristic (14:0)
  • Palmitic (16:0)
  • Stearic (18:0)
22
Q

What are the major sources of “bad” fat?

A
Butter 
Milk 
Meat 
Coconut 
Shortening 
Beef fat 
Chocolate
23
Q

What are the cholesterol lowering fats?

A
  • Linoleic acid (18:2)
  • a-loinolenic acid (18:3)
  • EPA (20:5)
  • DHA (22:6)
24
Q

What are the harmful effects of Trans-fats?

A
  • Dyslipidemia i.e. high LDL, low HDL, and high TG
  • Abdominal fat deposition
  • Systemic inflammation
  • Endothelial dysfunction
  • DM
  • Membrane effects (ROS)
25
Q

What is a Mono-unsaturated fat?

A

Single double bond

*****Also called “MUFAs” and liquid at room temp. b/c of higher melting point

26
Q

What are the mono-unsaturated fatty acids?

A
Palmitoleic acid (16:1) 
Oleic acid (18:1) 

*****Note that the most common source is olive oil

27
Q

What is a PUFA?

A

Fat with multiple double bonds

28
Q

What are Eicosanoids?

A
  • Signaling molecules
  • Made from oxidation of 20C FA

**Include prostacyclin, thromboxane, lipoxins, and leukotrienes

29
Q

What is the difference between Eicosanoids derived from FA with N6 or N3 oils?

A
N6= pro-inflammatory 
N3= less inflammatory
30
Q

Outline the pathogenesis of Athersclerosis.

A

1) Free radicals attack PUFAs and apoB generating fragments
2) LDL is not recognized by hepatocyte receptor
3) Scavenger receptors on macrophages bind LDL fragments and makes “foam cells”
4) Dead and dying foam cells deposit cholesterol creating atherosclerosis

Note that oxidized lipids also stimulate the inflammatory response*

31
Q

What are free radicals?

A

Unstable atoms with unpaired electrons

32
Q

What are the defense mechanisms against free radicals?

A
  • Protective cellular enzymes
  • Fat-soluble anti-oxidants
  • Proteins and metabolites that protect the aqueous environment of cells
33
Q

What are the protective cellular enzymes that inactive free radicals?

A

Superoxide dismutase

Catalase

34
Q

What are the cardioprotective fat-soluble anti-oxidants?

A

Alpha-tocopherol

Carotenoids

35
Q

What proteins and metabolites protect the liquid environment of cells?

A

Albumin
Uric acid
Ascorbid acid

36
Q

Is there a difference in the efficacy of different sources of anti-oxidants?

A

Generally, fruits, veggies, seeds, and nuts are better than corresponding supplements

37
Q

How many servings of cold water fish per week have been shown to be cardioprotective?

A

2