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Clinical Nutrition 1 > Hypertension Part II > Flashcards

Hypertension Part II Flashcards

1
Q

PA recommendations HTN

A

Accumulation of moderate PA of 30-60mins/day on most days (4-7 days) in addition to daily living activities. Increasing PA should be GRADUAL to avoid stressing out the heart

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2
Q

Nutriton Diagnosis HTN

A
  • Excessive E
  • Excessive fats
  • Excessive sodium
  • Inadequate PA
  • Overweight/obese
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3
Q

Nutrition Intervention HTN (What to do in conjunction with anti-hypertensives?)

A
  • DASH
  • Weight-loss
  • Sodium
  • Increase K+/Ca2+/Mg2+
  • PA
  • Smoking cessation
  • Stress management
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4
Q

Key nutrients to increase in HTN

A
  • Potassium
  • Magnesium
  • Calcium
  • Fibres
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5
Q

Weight-loss of 10-15%

A

SBP decrease by 5-20 mmHg

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6
Q

DASH diet

A

SBP decrease by 8-14 mmHg

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7
Q

Lower sodium diet

A

SBP decrease by 2-8 mmHg

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8
Q

Sources of fibre/energy

A

Whole grains

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9
Q

Sources of K+/Mg/Fibre

A

Dark green and orange veg, apples, apricots, grapes, tangerines

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10
Q

Sources of calcium/protein

A

Low-fat dairy

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11
Q

Sources of protein/Mg

A

Lean trimmed meats, opt for broil/poach/roasted poultry

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12
Q

Sources of energy/fibre/protein/mg2+

A

Nuts, lentils, legumes

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13
Q

How was DASH diet evidenced to be effective against HTN?

A

When compared to control, and control with high fruit and veg, “mixed diet” (dash diet) showed negative correlation with BP

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14
Q

What happened when subjects consumed the high fruits/veg control diet (SAD diet but more fruits and veg)

A

Saw 1/2 amounts of decreased BP compared to DASH diet

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15
Q

Is dash-diet a sodium restrictive diet?

A

NO

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16
Q

DASH diet - sodium =

A

Moderate

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17
Q

Dash diet - potassium =

A

High

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18
Q

DASH diet - calcium =

A

Meet DRI

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19
Q

DASH diet - magnesium =

A

HIGH

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20
Q

DASH diet - fibre =

A

HIGH

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21
Q

DASH diet - fat AMDR =

A

27%

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22
Q

DASH diet - SFA AMDR =

A

6% (low)

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23
Q

DASH diet - protein AMDR =

A

18%

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24
Q

DASH diet - CHO AMDR =

A

55%

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25
Q

What would be the first dietary intervention?

A

Switch to DASH like diet, THEN reduce sodium intake to the UL

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26
Q

(T/F) Once all patients start DASH diet, they should work towards consuming a low-sodium dash diet

A

False, unless they have refractory HTN (all other lifestyle mods without reaching target goals)

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27
Q

What did the Omni-heart study reveal?

A

That DASH diets rich in protein and rich is unsaturated FA (Mostly MUFA) further reduced BP in hypertensive individuals, but increasing CHO did not.

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28
Q

What were the effects of high-fat/low-CHO DASH diet?

A
  • Similar decrease in BP
  • Deceased TG
  • Decrease large/medium VLDL
  • Did NOT decrease LDL, but increased diameter (less atherogenic)
29
Q

What does the HF/LC DASH diet suggest?

A

That low fat dairy products may not be required to reap benefits (recall SFA and dairy does not increase CVD risk), and patient can consume “high” fat of they do not need to lose weight

30
Q

Ultimately, what does the DASH diet do?

A

Deceased BP and CVD risk

31
Q

What is first-line treatment?

A

Medications

32
Q

What is ALWAYS recommended to go with first-line treatment?

A

Health behavioural management

33
Q

In Low-risk patient (no TOD or CVD risk) what is the threshold to begin drug treatment?

34
Q

In patient with TOD or CVD risk factors, what is the threshold to begin drug treatment?

35
Q

In the very elderly, what is the threshold to begin drug treatment?

A

160 (Due to high risk:benefit ratio)

36
Q

Why increase threshold for elderly HTN treatment?

A

Since side-effect may be more serious than benefits, and does not have an optimal risk:benefit ratio

37
Q 
Arrange the following anti-HTN in order of prescription:
Single-Pill combination
ACE-1
B-Blockers
ARB
Thiazide/Loop-diuretics
Calcium Channel Blockers
A 
Thiaide/Loop-diuretics
ACE-1
ARB
Calcium Channel Blockers
B-Blockers
Single-Pill combination
38
Q

(T/F) When a patient is not responsive to a medication, physician may add on another medication rather than increasing dosage

A

True - better to act on more than one mechanism and is the rationale behind the single-pill combination

39
Q

What are some considerations when prescribing anti-hypertensives?

A
  • Metabolized by kidney and liver –> Issues with organs?
  • Drug/nutrient interaction –> Avoid natural licorice, grapefruit
  • Nutritional status –> Low albumin may impact drug transport
  • Physiological status –> Age, pregnancy, lactation
40
Q

anti-HTN appropriate for diabetics? (ADA)

A

ACE-I
Diuretics
ARB

41
Q

anti-HTM appropriate for Coronary Artery Disease?

A

All but diuretics

42
Q

What should NOT be used in Heart Failure?

A

Calcium channel blockers

Diuretics

43
Q

Mechanism of loop/thiazide diuretics

A

Decrease Na+/K+ reabsorption and cause osmotic diuresis. Na, K+ and H+ losses, must monitor potassium levels –> Risk of HYPOKALEMIA

44
Q

K-sparing diuretics mechanism

A

Inhibit aldosterone, less Na+ into blood stream while retaining potassium. Risk of HYPERKALEMIA if taking supplements at the same time

45
Q

Loop diuretics example

A

Furosemide/Lasix

46
Q

Loop diuretics side-effects

A

Hypokalemia, hyperglycemia, anorexia

47
Q

Thiazide diuretic examples

A

Hydrochlorthiazide/Apo-Hydro

48
Q

Thiazide diuretic side-effects

A

Hypokalemia, hyperlgycemia, anorexia, malaise, muscle weakness

49
Q

Guidleines for booth loop/thiazide diuretics? (K losing)

A

Provide potassium rich foods or supplementation (Note supplements could induce N/V - take with food)

50
Q

K+ SPARING diuretics example

A

Spirinolactin (Aldactone), Triamterene, Amiloride

51
Q

Guideline for K+ sparing diuretics?

A

AVOID EXCESS POTASSIUM THROUGH DIET AND SUPPLEMENTATION. Avoid salt-supplements, excess water, natural liquorice and take with food.

52
Q

Should those on K+ sparing diuretics reduce consumption of dietary potassium?

A

No, but don’t consume in excess amounts

53
Q

ACE-I example

A

Ramipiril/Altace

54
Q

ACE-I mechanism

A

Inhibits conversion of Ang I –> Ang II, decreases vasoconstriction and vasopressin/aldosterone release

55
Q

ACE-I side effects

A

Hypotension, dry cough, decreased renal function, hyperkalemia. Side effects exacerbated in African-Americans?

56
Q

Ace-I guidelines

A

Avoid salt-substitutes and natural liquorice

57
Q

When would ARB be prescribed? What it it? What effect?

A

When ACE-I cannot be tolerated.
Ang II blocker
Same downstream effects of ACE-I

58
Q

ARB mechanism

A

Blocks the binding of ANG-II to receptors, decrease vasoconstriction and vasopressin/aldosterone release

59
Q

Side effects of ARB

A

Hyperkalemia, N/V

60
Q

ARB guidelines

A

Avoid salt-substitutes, natural liquorice, grapefruit

61
Q

Long acting CCB examples

A

Amlodipline/Norvasc

62
Q

CCB mechanism

A

Affect movement of Ca through channels, cause vasodilation and inhibit contraction of myoepithelium

63
Q

CCB side effects

A

Edema, nausea, heartburn (GERD?)

64
Q

CCB guidelines

A

AVOID IN HF, limit caffeine, avoid completely

65
Q

Which CCB should grapefruit be avoided?

A

Felodipine/Plendil

66
Q

B-blocker examples

A

Proponolol/Atenolol/Metoprolol

67
Q

B-blocker mechanism

A

Block B-adrenergic recpetor in heart (epi/norepi), decrease CO and heart rate .

68
Q

What are the severe side effects of B-blocker?

A

Can mask/mimic symptoms of hypoglycemia, dangerous for those w/ DM. Dizziness, fatigue, CHF, hallucinations, insomnia.

69
Q

B-blocker guidelines

A

Caution with DM, avoid natural liquorice and NOT recommended as initial therapy for those over 60 y/o.

Clinical Nutrition 1 (30 decks)

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