Nutrition Module 10: CVD - HT and Other Risk Factors Flashcards

1
Q

What does BP refer to? What are the 2 factors that contribute to it?

A

Mean arterial pressure:

  1. Cardiac output
  2. Systemic vascular resistance
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2
Q

Common presentation of HT?

A

Normal cardiac output

with systemic vascular resistance

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3
Q

What 3 factors can affect systemic vascular resistance? Does each increase or decrease it?

A
  1. Norepi (as an NT and circulating hormone): INCREASE
  2. NO: DECREASE
  3. Elasticity loss with aging: INCREASE
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4
Q

What are the 8 risk factors of HT?

A
  1. Obesity
  2. DM
  3. Age above 65
  4. Low SES
  5. Sedentary lifestyle
  6. Ethnicity = AA or hispanic
  7. Alcohol abuse
  8. Family history
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5
Q

What % of americans have elevated BP or are taking meds for it?

A

33%

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6
Q

How does BP increase the risk for CVD?

A

CVD risk increases doubles for each 20/10 increment

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7
Q

How can diet modifications lower BP?

A

By more than 20/10 mmHg

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8
Q

By how much is the risk of stroke increased for people with untreated HT?

A

2-3x

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9
Q

What are the 5 criteria to make a metabolic syndrome diagnosis? How many of these need to be met?

A

3 out of the 5:

  1. Elevated waist circumference
  2. High TAGs
  3. Low HDLs
  4. High BP
  5. High FBG
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10
Q

What is another name for metabolic syndrome? What can this other name also refer to though?

A

Syndrome X

Can refer to a problem with heart rate regulation

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11
Q

What diseases are metabolic syndrome closely associated with?

A

T2DM and CVD

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12
Q

What are the 3 underlying contributing factors of metabolic syndrome?

A
  1. Obesity
  2. Insulin resistance
  3. Sedentary lifestyle
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13
Q

What 4 minerals play an important role in HT?

A
  1. Na
  2. Ca
  3. K
  4. Mg
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14
Q

What does it mean for someone to be salt-sensitive? What % of HT patients are salt-sensitive?

A

Their BP responds to dietary salt intake

50-60%

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15
Q

What is the definition of HT Stages 1 and 2? Note?

A

STAGE 1: 140-159/90-99

STAGE 2: 160+/100+

Note: numbers can be higher averaged over 2 or more visits

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16
Q

What 8 factors increase the effect of NaCl restriction on BP?

A
  1. Older peeps
  2. AAs
  3. High BP
  4. Genes
  5. Obesity
  6. Renal abnormalities
  7. Abnormal RAA system
  8. Low renin or slow renin response
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17
Q

How much does the typical American diet provide in sodium? What is the recommended intake?

A

2,300-4,700 mg

Rec: below 2,300 mg/day

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18
Q

Where does most of the sodium in the american diet come from? %?

A

Food processing: 75%

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19
Q

How much salt intake is consumed while cooking/eating?

A

10%

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20
Q

How much Na does table salt contain?

A

40%

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21
Q

By how much is BP decreased on average if following rec Na intake? How does this reduce CVD risk?

A

Reduces systolic BP 2-8 mmHg: 5-20% decrease in CVD risk

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22
Q

How does excessive salt intake impact cancer risks?

A

Increase stomach cancer risks

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23
Q

How many mmol does 2300 g of Na correspond to?

A

100

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24
Q

How does K+ affect BP? How? How can you fix this?

A

Hypokalemia = renin secretion = vasoconstriction = higher BP

Eat more potassium in fruits, veggies, fresh meats, and milk

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25
Q

What meds can cause K+ depletion? What other deficiency do they cause? Why?

A

Diuretic meds

Also thiamin deficiency because increased losses with urine

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26
Q

How does Ca2+ affect BP?

A

Deficiency causes high BP

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27
Q

How many servings of calcium rich food should you have each day to lower BP?

A

2-4

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28
Q

Can you just take supplements for the minerals that help with HT?

A

NOPE, not the same effects

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29
Q

How does Mg2+ affect BP?

A

Deficiency causes high BP

30
Q

How does alcohol affect HT?

A
  1. Increased mean arterial pressure
  2. Resistance to HT therapy
  3. Increased stroke risks
31
Q

What 6 cancer risks are higher with high alcohol intake?

A
  1. Mouth
  2. Esophagus
  3. Pharynx
  4. Larynx
  5. Liver
  6. Breasts
32
Q

What are the 2 proposed mechanisms for why obesity increases HT risk?

A
  1. Increases salt-sensitivity

2. Hyperinsulemia causes Na retention and catecholamine release

33
Q

What is an independent risk factor of HT?

A

Obesity

34
Q

Is weight loss as effective for lowering BP as first-line meds?

A

YUP

35
Q

How much exercise to lower BP?

A

3-4 times/week for 40 min each

36
Q

What kind of effect do caffeine and omega-3 FAs have on BP?

A

Minor effects

37
Q

By how much will the BP be lowered for every 10 kg = 22 lbs lost?

A

5-20 points

38
Q

By how much is HT risk increased for obese people?

A

2-6x

39
Q

Why are the 5 lifestyle interventions for HT?

A
  1. Lose weight as appropriate
  2. Regular aerobic PA
  3. DASH eating pattern to obtain adequate K+, Ca2+, and Mg2+
  4. Restrict Na
  5. Limit alcohol to 1 drink day for women and 2 for men
40
Q

What is the DASH eating pattern?

A

High fruits and veggies (9 servings/day) and low-fat dairy

41
Q

Should the 5 lifestyle changes for HT be done if drug therapy is indicated?

A

YUP

42
Q

BP for prehypertension?

A

Systolic: 120-139
Diastolic: 80-89

43
Q

Normal BP?

A

STAGE 1: Systolic: below 120

Diastolic: below 80

44
Q

What is the treatment for prehypertension?

A

Lifestyle modifications

45
Q

What is the treatment for HT Stage 1 and 2?

A

Lifestyle modifications + drugs

46
Q

How often should one eat cold water fish to cut the chances of dying from stroke in half?

A

1/week

47
Q

What are 6 cold water fish?

A
  1. Salmon
  2. Trout
  3. Herring
  4. Mackerel
  5. Sardines
  6. Halibut
48
Q

How many grams a day should patients with established heart disease eat omega-3 FAs?

A

1g/day

49
Q

What are the 5 reasons for omega-3 FAs to reduce CVD risks?

A
  1. Reduce TAGs
  2. Moderate tachychardia and arrhythmia
  3. Inhibit platelet aggregation
  4. Lower BP
  5. Prevent plaque formation in coronary artieries
50
Q

What are the main 3 differences between omega 3 and omega 6 eicosanoids?

A
  1. Omega 3 more vasconstrictive
  2. Omega 6 more immunosuppressive
  3. Omega 6 induce platelet aggregation
51
Q

What leads to platelet aggregation? 2 factors

A

Cytokine secretion by cells in vascular lesions

  1. Chronic
  2. Acute (catecholamines)
52
Q

How does factor VII affect CVD risk? What causes this?

A

High fat intake = high factor VII = high blood coagulation cascade = increased CVD risk

53
Q

How does Vitamin K play a role in coagulation?

A

A lot of the proteins in the coagulation cascade are vitamin K dependent

54
Q

Where do we get our Vitamin K from?

A
  1. Intestinal bacteria

2. Diet

55
Q

What can cause Vitamin K deficiency?

A

Oral antibiotics

56
Q

What drugs are given to patients with high risk for thrombosis? Who are these patients?

A

Patients with mitral valve damage or artificial heart valves: coumadins = VK antagonists like warfarin

57
Q

What should coumadin treatment be accompanied by?

A

NORMAL/CONSTANT Vitamin K intake

58
Q

How does vitamin K affect CVD risk?

A
  1. Low Vitamin K best to reduce coagulation and thrombosis risks
  2. Vitamin K necessary to control arterial calcification
59
Q

What 2 factors often combine to cause increased homocysteine levels?

A
  1. Genetic variant of an enzyme in homocysteine metabolism

2. Lack of folate, B6, B12, or riboflavin

60
Q

Is there evidence that homocysteine lowering interventions with vitamin supplements prevent CVD events?

A

NOPE

61
Q

Which is more bioavailable: synthetic or natural folate?

A

Synthetic

62
Q

What is the form of naturally occurring folate?

A

Folylpolyglutamate

63
Q

What is the form of synthetic folate?

A

Free folic acid

64
Q

How is homocysteine generated in the body?

A

Methionine => SAM => s-adenosylhomocysteine + methylated compound => homocysteine

65
Q

How are homocysteine concentrations kept low?

A
  1. Methyl transferase: 5-methyltetrahydrofolate + homocysteine + B12 => tetrahydrofolate + methionine
  2. Cystathionine beta-synthase: homocysteine + B6 + serine => cystathionine + B6 => cysteine + alpha-ketoglutarate + NH4+
66
Q

What are the 5 toxic effects of homocysteine in tissues and blood?

A
  1. Endothelial cell damage
  2. Cholesterol oxidation
  3. Oxidation of apolipoproteins: more atherogenic
  4. Platelet adhesion and aggregation
  5. NO scavenging = inhibition of vascular motility
67
Q

How does NO react with homocysteine to increase CVD risks?

A

They react together = s-nitrosohomocysteine =NO availability decreased = decreased vasodilation + lack of NO in platelets: promotion of venous and arterial thrombosis

68
Q

How is NO synthesized in endothelial cells?

A

NO synthase: arginine => citrulline + NO

69
Q

How can bleeding related to antiobiotic use be prevented?

A

Consumption of cooked greens and green veggies

70
Q

Other than homocysteine what else can interfere with NO?

A

Oxidized lipids and lipoproteins

71
Q

How can serum [K+] affect BP?

A
  1. High K+: increase BP through RAA system

2. Low K+: increases BP through renin and vasoconstriction