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NUTR 344 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

HTN is the major risk factor for __

A

HTN is the major risk factor for cardiovascular disease

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2
Q

What is the effect of low potassium intake on sodium levels

A

low potassium intake results in sodium retention

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3
Q

What is sodium sensitivity?

A

an increase in blood pressure in response to a higher sodium chloride intake than that in the baseline diet

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4
Q

Human kidneys are poised to __ sodium and __ potassium.

A

Human kidneys are poised to conserve sodium and excrete potassium.

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5
Q

aldosterone and sodium levels

A

aldosterone results in sodium retention

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6
Q

how does excess of sodium and deficit of potassium lead to an increase in arterial and arteriolar smooth-muscle tone

A

Deficit K leads to an inhibition of Na+/K+ ATPase (sodium pump) and the potassium channel in the smooth muscle cell

The inhibition of the sodium pump and the resulting stimulation of the sodium–calcium exchanger type 1 (NCX1) increase the intracellular concentration of calcium that in turn triggers actin–myosin interaction and stimulation of vascular contraction.

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7
Q

What are the major forms of cardiovascualr disease

A

§ Hypertension

§ Atherosclerosis
§ Ischemic heart disease

§ Peripheral vascular disease

§ Heart failure

§ Cerebrovascular disease

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8
Q

what is a CDV

A

it’s an umbrella term- a disease of heart and blood vessels

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9
Q

What are the leadign causes of death in canada?

A

Cancer

Diseases of the heart

Cerebrovascular diseases

Other

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10
Q

What are the cnages in the trends in prevalence of reported hypertension

A

In recent years high blood pressure became mor eprevalent in males than females, eventhough it used to be vise-versa before

  • might be due to higher obesity and overweight rate in males who are now became more susceptible to hypertension
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11
Q

How is age and sex related to the risk of HTN?

A

age is a risk factor
before the age of menopause, prevalence is lower in females
after the menopause, the risk in females becomes somewhat same as in males
then in 75+ males are lower at risk
this might be sue to the fact that there are more females who are older

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12
Q

Awareness and treament of HTN stats

A

65%- treated by hypertension and controlles

18%- unaware

14%- treated, not controlles

4%- aware, not treated

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13
Q
  • Hypertension is __ and __- Antihypertensives are one of the most __ drug categories
A

Hypertension is prevalent and costly- Antihypertensives are one of the most expensive drug categories

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14
Q

How many cnadians are affected by HTN

A

Affects >1 in 5 (≅22% of Canadian adults aged >20 y). Since 18% of individuals with hypertension are not aware of their condition, the true prevalence of hypertension is likely higher.

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15
Q

The lifetime risk for developing hypertension among adults aged 55 to 65 years with normal blood pressure is _%.

A

The lifetime risk for developing hypertension among adults aged 55 to 65 years with normal blood pressure is 90%.

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16
Q

What is the most common reason to visit a doctor?

A

HTN

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17
Q

What is the number one reason for taking meds?

A

HTN

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18
Q

Which rases are more/less susceptible to HTN?

A
  • African-americans ≅ 44%
  • Whites ≅ 33%
  • Hispanic ≅ 28%
  • Filipinos, Japanese ≅ 26%
  • Chinese, Korean ≅17%
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19
Q

Is there a genetic component to HTN

A

yes

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20
Q

Is HTN more prevalent in canada or US

A

US

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21
Q

How to calculate MAP?

A

mean arterial pressure = cardiac output X peripheral resistance

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22
Q

how to calculate cardiac output and what are the untis? what does it measure

A

CO (L/min) = stroke volume (L/beat) x heart rate (beats/min)

the volume of blood that the herat is pumphing per minute
unit: l/minute

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23
Q

How to calculate resistance? What are the units? How does vasoconstriciton adn vasolidation affect it?

A
  • resistance against which your heart is pumping the blood
  • radius has a bigger impact on the resistance over length or viscosity
  • (length of vessel x viscosity of the blood)/ (radius^4)
  • in vasoconstriction: resistance ↑
  • in vasodilation: resistance ↓
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24
Q

Wghat is Mean arterial pressure (MAP) is regulated by?

A

Sympathetic nervous system

Renin-angiotensin-aldosterone system
Renal function- fluid and electrolyte control
Hormones involved: epinephrine, vasopressin, angiotensin II

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25
Q

Factors Influencing Arterial BP

A

Cardiac output - heart rate x stroke volume

heart rate is regulated by ANS
Para and sympa
sympa actvity decreases HR
parasympathetic decreases HR
Sympathetic NS increases stroke volume by causing blood vessels to contract more

Stroke volume- amount of blood pumped by the heart
increases with sympathetic NS and epinephrin
Sympathetic NS increases stroke volume by causing blood vessels to contract more

venous blood- return of blood from periphery
the more blood returned- the higher the stroke volume
venous return increases with the activity of respiratory pump- helps blood to go from area of higher to lower pressure-> go back towards the heart

skeletal activity- contraction of the muscles against the veins which will help to bring the blood back up

cardiac suction effect
heart acts as a pump- contract and changes the pressure at the levels of the heart which pushes blood through the heart

venous volume is dependent on the effective blood volume
blood volume is controlled in short term by fluid shift in the compartments of the body;
in longe term -RAAS, kidneys, vasopressin and salt and fluid levels

Total peripheral resistance

resistance depends on the radius and viscosity; directly proportional to viscosity and inversely proportional to the radius
blood viscosity increases with the amount of RBC (higher Htc-> higher viscosity) .hematocrit is regulated within certain limit
muscles need more nutrients during the exercise- will make vessels expand- local regulatory control in the muscles

extrinsic vasoconstrictive control- sympathetic activity and epinephrin-> constriction of blood vessels
angiotensin and vasopressin result in the constriciton of blood vessels

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26
Q

Renin-Angiotensin-Aldosterone System (RAAS)

A

change in osmolarity of blood volume will tigger negative feedback
kidneys detect changes in the blood pressure- changes in electrolytes, fluid levels
they will release renin
renin will act upon angiotensiongen (inactive, released by the liver) and will convert it into angiotensin I
angiotensin I will reach the lungs where it will be converted into angiotensin II by angiotensin-converting enzyme (ACE)
angiotensin II will act on adrenal cortex and result in the release of aldosterone

aldosterone will act on kidneys to make more Na reabsorption by the kidney tubules; chloride will follow-> Na and Cl are conserved
osmosis will follow resulting in water reabsorption

angiotensin II acts on artery radius-> vasoconstriction-> increased blood pressure
also stimulates the thirst signal from hypothalamus-> increased fluid intake
stimulates vasopressin release from pituitary gland-> vasopressin acts on kidney tubules will increase water reabsorption

aldosterone acts both on water and electrolytes
vasopressin acts upon fluid mainly-> reabsorption

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27
Q

Target organ damage related to hypertension

A

heart: LVH (eft ventricular hypertrophy), CHD, CHF (congestive heart failure)

Brain: Hemorrhage, Stroke, dementia

Eyes: Retinopathy

Blood vessels: Peripheral Vascular Disease

Kidneys: Renal Failure, Proteinuria

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28
Q

How is the Measurement of BP done?

A

sphygmomanometer, in mmHg

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29
Q

What are the 2 types of causes of HTN?

A

§ primary/essential

§ secondary

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30
Q

Describe primary causes of HTN?

A

Primary/essential/ idiopathic (95% of cases)

  • Unknown etiology
  • Interaction from environmental and genetics factors
  • Influenced by dietary and behavioral factors
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31
Q

Describe secondary causes of HTN?

A

(5% of cases)
Occurs secondary to another condition such as renal, endocrine, or neurological disorders

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32
Q

What are the symptoms of HTN?

A

§Hypertension is typically asymptomatic (« silent killer »)- can go on untoticed for a long period of time

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33
Q

Major risk factors of HTN

A

Non-modifiable

  • Age >60 y
  • Men, postmenopausal women (due to lower levels of estrogen), ethnicity (African-American, Russians, Finns)
  • Family history of CVD : women <65 y or men <55 y- premature CVD

Modifiable

  • Smoking
  • Sedentary lifestyle
  • Abdominal obesity, insulin resistance
  • Excess sodium intake
  • Poor diet quality
  • Stress
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34
Q

Hypertension – Contributing Factors and Mechanisms

A
  • Excessive secretion of vasopressin and angiotensin II: ↑ vasoconstriction and fluid retention
  • Smoking: interferes with NO-> impairs endothelial vasodilation as NO usually helps vasodilation
  • Renal disease: reduced blood flow-> ↑ angiotensin IIàvasoconstriction + Na+, Cl-, water retention-> blood volume
  • Adrenal disorders: Adrenal disorders that ↑ secretion of epinephrine and norepinephrine -> vasoconstriction, ↑ cardiac output
  • Hyperinsulinemia is associated: mechanisms unclear
  • Neurological diseases
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35
Q

WHO Classification of HTN

A

* measured on 2 or more ocassions

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36
Q

Target organ damage and associated clinical conditions (ACC)- heart

A

Cardiovascular disease :
- Coronary artery disease : angina or prior MI

  • Left ventricular hypertrophy or dysfunction
  • Heart failure
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37
Q

Target organ damage and associated clinical conditions (ACC)- brain

A

Cerebrovascular disease
- Stroke or TIA (transcient ischemic attack)

  • Hemorrhage
  • Dementia
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38
Q

Target organ damage and associated clinical conditions (ACC)- eyes

A

retiopathy

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39
Q

Target organ damage and associated clinical conditions (ACC)- blood vessels

A

Peripheral artery disease

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40
Q

Target organ damage and associated clinical conditions (ACC)- nephrones

A

§ Albuminuria
§ Chronic kidney disease

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41
Q

What are the characteristics of a low risk-patient?

A

No target organ damage ot cardiovascular risk factros

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42
Q

What are the characteristics of a moderate-to-high risk factor patient?

A

multiple cardiovascular risk factros & 10-year global risk < 15%

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43
Q

What are the characteristics of a high risk factor patient?

A

Individuals with one or more of the following clinical indications should consent to intensive management:

  • Clinical or sub-clinical cardiovascular disease

OR

  • Chronic kidney disease

OR

  • Estimated 10-year global cardiovascular risk ≥15%

OR

  • Age ≥75 years
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44
Q

Hypertension Canada High-Risk Patient BP cutoffs for initiaiton of antihypertensive therapy and BP treatment target

A
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45
Q

BP measurement methods

A

Office:

  • Preferred: Automated office blood pressure (AOBP)- Oscillometric (electronic)
  • Non-automated (manual) office BP” Non-AOBP Auscultatory (mercury)

Office Automated (unattended, AOBP)

  • Oscillometric (electronic)
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46
Q

Out of office BP measurement methods:

A

Ambulatory (ABPM)

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47
Q

Hypertension Diagnostic Algorithm

A

1) If AOBP is used, use the mean calculated and displayed by the device. If non-AOBP (see note 2) is used, take at least three readings, discard the first and calculate the mean of the remaining measurements.
4) Serial office measurements over 3-5 visits can be used if ABPM or home measurement not available.
5) Home BP Series: Two readings taken each morning and evening for 7 days (28 total). Discard first day readings and average the last 6 days.
6) Annual BP measurement is recommended to detect progression to hypertension.

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48
Q

Hypertension treatment goals

A

Reduce risk of CD and renal disease; and target organ damage

Lower BP to clinically appropriate level

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49
Q

Hypertension – Comprehensive Treatment plan includes:

A
  • Physical activity
  • Weight reduction
  • Nutrition therapy
  • Moderation in alcohol, relaxation therapy, smoking cessation
  • Pharmacological interventions: loop diuretics; thiazides; carbonic anhydrase inhibitors; potassium sparing diuretics

!!!pills are never used on their own!!!

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50
Q

Dietary factors involved in hypertension

A
  • High calories, excess weight, obesity
  • Sodium- big infuence
  • Potassium- big influence
  • Calcium
  • Magnesium
  • Alcohol
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51
Q

Obesity and hypertension in adults <55 y.o

A

§ Direct link between excess weight and HTN

§ 60% of those with excess weight and normal BP will develop HTN in the next 4 years

§ Abdominal obesity is more associated (than just obesity/ subcutaneous fat)

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52
Q

causes of HTN associated with obesity

A

§ Insulin resistance/hyperinsulinemia

§ Overactivity of the sympathetic nervous system

§ Alterations in the RAAS

§ Leptin increases sympathetic activity; this function is preserved with leptin resistance- the effect leptin has on HTN is still the same even if leptin resistance has been developed

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53
Q

What is the most potent non-pharmacological approach for HTN treatment?

A

weight loss

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54
Q

How does weigth loss affect HTN?

A
  • Reduced BP is measured even before healthy weight is reached: 5-20 mmHg per 10 kg loss
  • Weight loss is indicated both in treatment and prevention of HTN
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55
Q

Recommendations for weight loss for HTN

A
  • Aim for BMI ≤ 25 kg/m2 + waist circumference <102 cm men, <88 cm in

women

  • All overweight patients should achieve a weight loss of 5 kg (↓ SPB by 4.4 and DPB by 3.6 mmHg) to reduce BP and risks for organ damage.
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56
Q

Weight loss approaches, when can it be difficult?

A
  • Diet education and instruction
  • Increase physical activity
  • Behavior modification
  • Weight loss may be more difficult if patient is using β-blockers beta blockers decrease heart rate-> decrease metabolic rates
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57
Q

Effect of sodium intake on Systolic blood pressure and urinary sodium excretion

A

For every increase of 100 mmol Na/d consumed-> increase in 3-6/0-3 mmHg SBP/DBP

the more you consume Na-> the more you will excrete
because of this Na regulation
sodium levels and excretion is tightly regulated
sodium excretion levels were used as a marker of sodium intake-> calculated the number of moles ingested
increases in blood pressure related to sodium excretion levels were noted

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58
Q

decrease in Na intake has a biggger impact on decreasing blood pressure in __ indivduals than in __ individuals

A

decrease in Na intake has a biggger impact on decreasing blood pressure in hypertensive indivduals than in normotensive individuals

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59
Q

What is the marker of sodium intake

A

number of moles pf sodium excreted

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60
Q

What is mean arterial pressure determined by?

A

cardiac output and total peripheral resistance

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61
Q

How is arterial blood pressure regulated?

A

Arterial blood pressure (BP) is regulated by the sympathetic nervous system, the renin–angiotensin–aldosterone system (RAAS), and renal function.

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62
Q

What does cardiac output equal to?

A

Cardiac output is equal to heart rate multiplied by stroke volume

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63
Q

What is heart rate dependent on?

A

Heart rate is dependent upon the balance between parasympathetic activity, which decreases heart rate, and sympathetic activity, which increases heart rate. The parasympathetic nervous system communicates with both the SA and AV nodes via the neurotransmitter acetylcholine, resulting in a decrease in heart rate. The sympathetic fibers, which are part of the cardiac accelerator nerves, stimulate the SA node and ventricles. When stimulated, these fibers release norepineph- rine, which causes an increase in heart rate

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64
Q

WHat does total peripheral resistance depend on?

A

The degree of resistance is dependent upon three factors: the radius of all arterioles, the length of the vessel, and the blood viscosity

Arteriolar radius is the most important factor in determining peripheral resistance.

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65
Q

What is the effect of Skeletal muscle activity on arteriolar radius?

A

Local metabolic controls in skeletal muscles may cause vasodilation, decrease resistance, and increase blood flow to those muscles in order to match metabolic needs.

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66
Q

The effect of Sympathetic activity and epinephrine on blood vessels

A

Sympathetic activity and epinephrine can cause vasoconstriction and increase resis- tance.

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67
Q

Vasopressin and angiotensin II effect on resistance and BP

A

Cause vasoconstriction-> decreased radius-> increased resistance

When there is a water deficit, vasopres- sin, released from the posterior pituitary gland, causes an increase in the reabsorption of water in the kidneys’ distal tubules. This will increase blood volume, thus increasing BP

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68
Q

What are the disease related death assocaited with high sodium intake?

A

High sodium intak eincreases the risk of CHD, CVD and ALL-cause mortality

this risk is higher with high sodium intake

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69
Q

Comparison of the effects of DASH-Sodium diet vs. standard American diet at 3 levels of sodium intake results

A

Movign from high intake to med intake of Na showed a smaller decrease in BP vs when goingr from med to low intake in both US and DASH diets

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70
Q

Wil the reduction of sodium intake always show an improvement in SBP?

A

Overall yes, btu individual response may vary- in non responders SBP may even increase

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71
Q

What are the demographics of reduced soidum intake responders

A

African-American Middle-aged
HTN, diabetes, renal

72
Q

Factors involved in heterogeneous responses to sodium reduction

A

◦ Familial/genetic factors

◦ Age
◦ Severity of hypertension

◦ Degree of restriction

◦ Renin-angiotensin-aldosterone (low renin) -> increased salt sensitivity

◦ Sympathetic response (high norepinephrine response)

◦ Duration of trials

73
Q

What is the effect of potassium on Na sensitivity?

A

↑ K intake-> ↓ Na sensitivity

74
Q

Dietary sodium DRI

A

Adequate intake (AI) :

14-50 y: 1500 mg Na/day

51-70 y: 1300 mg/day

71+ y: 1200 mg/day

Upper limit (UL): 2300 mg Na/day for all adults

75
Q

Do canadians exceed sodium intake recommendations?

A

The majority of Canadian adults exceeds the tolerable limit of 2300 mg/d

Average total intake = 3400 mg/day

76
Q

The 2014 Canadian Hypertension Education Program (CHEP) recommends: (salt intake)

A

To decrease blood pressure, consider reducing sodium intake towards 2,000 mg (5 g of salt or 87 mmol of sodium) per day

a bit less than a teaspoon -> 1/2 tsp of salt has about 1,150 mg of sodium

77
Q
A
78
Q

What are the major sources of salt in our diets?

A

80% of average sodium intake is in processed foods- mostly bread, processed meats, soups, cheese, milk products

Only 10% is added at the table or in cooking

79
Q
A
80
Q

Reading the Nutrition Fact Label tips to lower salt intake

A

Read the information on food packages

  • Buy unsalted and lower sodium foods whenever possible.
  • Look for words such as sodium-free, low sodium, reduced sodium, or no added salt on the package.

Compare food labels

  • Check the serving size and note the amount of sodium.
  • Choose foods with less than 120 mg sodium per serving.
  • Choose foods with sodium that have a % Daily Value (DV) of 5% or less.
81
Q

Do we recommend diets that prvide less than 1000mg of NA

A

no

82
Q

What are the 3 types of sodium controlled diets?

A

3000 mg Na

  • Eliminate high Na processed foods and beverages (fast foods, salad dressings, smoked meats, kosher meats, canned foods).
  • Up to 0.25 tsp salt permitted during cooking or added at table

2000 mg Na

  • Eliminate processed and prepared foods and beverages high in Na. Limit milk and milk products to 2 cups/d. No salt in preparation of foods or added at table

1000 mg Na

  • Same as above. Omit canned, frozen, deli foods, cheeses, margarines. Limit regular bread to 2 servings/d.
83
Q

What are the benefits of reduced salt intake?

A
  • Reduces BP
  • Prevents hypertension
  • Has an additive effect to antihypertensive medications-> lower doses and better control
  • Reduces risks of complications
84
Q

Describe Sodium Reduction in Processed Foods in Canada

A

In 2012, Health Canada published voluntary targets to reduce sodium in processed foods by end of 2016

◦ Consultation with food industry, health sector and research experts
◦ To encourage sodium reduction while maintaining food safety, quality and consumer acceptance

Results:

Only 14% of food categories met the targeted reduction.

48% did not make any meaningful progress toward sodium reduction; in fact, among the 48%, the sodium levels in several categories increased. In terms of the saltiest products on the market, only 30% lowered sodium content to levels similar to other foods in the same category.

85
Q

What is the effect of potassium on blood pressure and HTN?

A

Inverse relationship between K intake and blood pressure:

  • decreased mean blood pressure
  • decreased prevalence of HTN with higher K intake
86
Q

Potential mechanisms of potassium influencing blood pressure

A

◦ Natriuresis-> Na is excreted by kidneys

◦ Suppressed renin (renin ultimately leads to an increased blood pressure)
◦ Attenuates vascular contraction-> vasodilation
◦ May reduce sympathetic activity and angiotensin II

87
Q

Impact of K on genetic inheritace of HTN

A

Protects against familial susceptibility

88
Q

How are intake levels of K and Na connected?

A

Effect of K is inter-dependent with sodium

◦ The greater the increase in BP with Na, the greater the decrease with supplemental K

89
Q

Potassium – Sodium relationship graph + explanation

A

Na favours K excretion - the higher the Na intake, the less efficeint our bodies are at conserving potassium
K favours Na excretion

90
Q

describe how does the modern western diet lead to hypertension

A

Modern western diet is characterized by high sodium intake and low potassium intake

Hign Na intake + Lack of renal adaptation and other defects in Na excretion leads to Ineffective K conservation which exacerbates low K intake, which is also made worse by Excessive renal and fecal K loss-> Deficit in K in the body

Deficit in K in the body results in greater Retention of Na by the kidneys -> Excess of Na in the body-> Extracellular fluid volume expansion-> Release of digitalis-like factor (inhibitor of Na, K ATPase)

This leads to exces cellular Na and deficit cellular K-> Vascular smooth-muscle cell contraction-> Increased peripheral resistance-> Hypertension

91
Q

Human kidneys are poised to conserve __ and excrete __.

A

Human kidneys are poised to conserve sodium and excrete potassium.

92
Q

Aldosterone contributes to the retention of __ by the kidneys.

A
93
Q

Mechanisms of increased sodium retention in hypertension :

A

1) Sodium–hydrogen exchanger type 3 is located in the proximal tubule and the thick ascending limb of the loop of Henle, where the bulk of filtered sodium is reabsorbed.
the activity of this transporter increases in hypertension, transporting more Na+ back into the tubule
2) Moreover, potassium depletion enhances sodium–hydrogen exchanger type 3 by inducing intracellular acidosis and by stimulating the sympathetic nervous system and the renin–angiotensin system
3) The sodium–chloride cotransporter in the distal tubule, the epithelial sodium channel in the collecting duct, and the sodium pump are activated by the aldosterone excess in primary hypertension, thereby promoting sodium retention and potassium loss. A high-sodium diet increases potassium excretion by increasing distal sodium delivery.
4) An endogenous “digitalis-like factor,” is released by the adrenal glands and the brain in response to a high-sodium diet. Digitalis-like factor mediates sodium retention by increasing the activity and expression of the renal sodium pump
5) Contrary to its short-term effects, the long-term effect of potassium depletion is to stimulate the activity and expression of the renal sodium pump, thereby promoting sodium retention

94
Q

HTN EFFECTS ON THE ARTERIAL WALL

A

Sodium retention, by means of the release of digitalis-like factor, and a potassium deficit or hypokalemia inhibit the sodium pump of arterial and arteriolar vascular smooth-muscle cells, thereby increasing the sodium concentration and decreasing the potassium concentration in the intracellular fluid
Increased intracellular sodium stimulates the sodium–calcium exchanger type 1 in the membrane, driving calcium into cells. A deficit of potassium in the body or hypokalemia inhibits potassium channels in the cell membrane, depolarizing the membrane (the membrane potential shifts closer to 0). Because of its electrogenic nature, the inhibition of the sodium pump itself decreases the membrane potential. Membrane depolarization in the vascular smooth-muscle cells promotes a further rise in intracellular calcium by activating voltage-dependent calcium channels in the membrane, calcium channels in the sarcoplasmic reticulum, and the sodium–calcium exchanger
The increased cytosolic calcium caused by these mechanisms triggers contraction of the vascular smooth muscle.

95
Q

Do canadians consume enough potassium?

A

Average K intake in Canadian adults:

◦ About 2800 mg/d in women ◦ About 3300 mg/d in men

Below DRI of 4700 mg/d

96
Q

What is the recommended intake of K and why?

A

Daily dietary intake of K should be ≥ 60 mmol (2300 mg)àassociated with decreased risk of stroke mortality

97
Q

What is the effect of the daily intake of + 50 mmol (2000 mg) of potassium?

A

+ 50 mmol (2000 mg)à -3.4/-1.9 mmHg BP

98
Q

Is K supplementation recommended as means of reduign blood pressure/treatign hypertension?

A
  • For normotensive people obtaining 60 mmol of dietary K daily,
    K supplementation is not recommended as a means of preventing high blood pressure
  • K supplementation above daily dietary intake of 60 mmol/d is not recommended as a treatment for hypertension
  • K supplements may be useful if diuretic-induced hypokalemia
99
Q

How can sufficent K intake be achieved?

A

Following Canadian Food Guide: emphasizing fruits and vegetables allows for sufficient K intake

100
Q

Risk factors for hyperkalemia

A
  • Patients using renin-angiotensin-aldosterone inhibitors
  • Patients receiving other drugs causing hyperkalemia
  • Chronic kidney disease (glomerular filtration rate <60 mL/min/1.73^2) -disrupts excretion and balancing pathways
  • Baseline serum potassium >4.5 mmol/L
101
Q

hyperkalemia- supplement and dietary intake of K recommendations

A

Do not advise increasing intake or taking supplements

102
Q

Calcium intake is __ associated with blood pressure

A

Calcium intake is inversely associated with blood pressure

103
Q

Potential mechanisms of increased calcium intake on decreased BP

A
  • ↑ sodium excretion
  • ↑ sensitivity to nitric oxide (NO)àvasodilation
  • Reduced production of superoxyde and prostanoids (vasoconstrictors)
104
Q

Recommendations: Calcium

A
  • For normotensive people Ca supplementation above the recommended daily intake is not recommended as a means of preventing high blood pressure
  • Ca supplementation above daily recommended dietary intake is not recommended as a treatment for hypertension
  • Using CFG and consuming 2-3 servings of milk products daily is sufficient
105
Q

Magnesium effects on BP and mechanism

A
  • Inverse relationship between Mg intake and blood pressure
  • Potential mechanisms relate to the role of Mg in vascular structure and function : regulates vascular reactivity and contractility-> has protective effect
106
Q

Mg intake and supplementation recommendations

A

◦ Increase dietary intake to reach DRI (men: 420 mg/d; women: 320 mg/d)

◦ Supplement above DRIs are not recommended

107
Q

effect of alcohol on BP

A
  • Dose-response relationship between alcohol intake over 2 drinks/d and increased blood pressure
  • Alcohol intake has an immediate vasovagal effect (↓ BP) but followed by elevated BP in the next 10-15 h.

Potential mechanisms:

  • Stimulation of sympathetic nervous system
  • Stimulation of cortisol secretion
  • Increased Ca uptake by cell membranes

Moderate alcohol consumtion does not raise BP and has cardioprotective effects

108
Q

Recommendations: Alcohol

A

àLimit to 2 drinks per day (men) àLimit to 1 drink per day (women)

Standard drinks:
◦ Beer: 360 mL (12 fl oz) 5%
◦ Wine: 150 mL (5 fl oz) 12%
◦ Spririts: 45 mL (1.5 fl oz) 40%

109
Q

To convert mg into mEq:

A

mg/atomic weight x valence = mEq

110
Q

Afterload definition

A

the resistance against which the ventricles of the heart must contract in order to eject blood into the systemic circulation

111
Q

cerebrovascular accident (CVA) definitoin

A

a stroke

112
Q

What are the vasopressin levels in hypertension

A

they are often elevated

113
Q

Hypertension Treatment Guidelines

A
114
Q

What are the primary stages of HTN treatment?

A

Increased physical activ- ity, smoking cessation, and weight loss, as well as reduction of sodium and alcohol intake

115
Q

Common nutrition diagnoses for individuals with hypertension

A

Common nutrition diagnoses for individuals with hypertension include excessive energy intake; excessive or inap- propriate intake of fats; excessive sodium intake; inadequate calcium, fiber, potassium, or magnesium intake; overweight/ obesity; food- and nutrition-related knowledge deficit; and physical inactivity.

116
Q

Brief Nutrition Counseling for Hypertension: Steps in Behavioral Counseling (“5 A’s”)

A
  • Assess (Food and Nutrient Intake, Knowledge/Beliefs/Attitudes, Behavior, Physical Activity and Function, and Biochemical Data)
  • Advise- Give clear, specific, and personalized behavior change advice.
  • Agree- Collaborate with patient to select treatment goals and methods.
  • Assist- Help patient acquire knowledge, skills, and support for behavior.
  • Arrange-Schedule follow-up appointments.
117
Q

Exercise and hypertension

A
  • -Accumulation of moderate physical activity of 30-60 minutes/day on most days (4-7 d/week), IN ADDITION to daily activities: reduces BP by 4-9 mmHg
  • Higher intensities are not more effective in reducing BP
  • Gradually increasing PA:
    • decreases the relative workload on the heart (as heart muscle is trained-> becomes more efficient): benefit for all CVD
    • May help reduce weight or maintain
  • For stage 1 HTN: resistance exercise does not negatively impact BP
  • Recommend gradual increase to 30-60 minutes/day of moderate intensity.
  • avoid heavy weigth as you tend to not breath-. escessive pressure on CV system
    high reps + light weight is recommended
118
Q

Nutrition Therapy for Hypertension – Assessment components

A

Identify dietary factors and patterns- eating out; nutritional knowledge
Evaluate need for weight control- normal weight-> no weight loss; excessive weight-> weight loss
Prioritize methods to meet DASH dietary goals

119
Q

What is the fundamental base of nutirional treatment of HTN

A

DASH

120
Q

Nutrition Therapy for Hypertension – Diagnosis

A

You need to identify nutritional causes of HTN

  • Excessive energy intake
  • Excessive or inappropriate intake of fats
  • Excessive sodium intake
  • Inadequate calcium, fiber, potassium, or magnesium intake -> beign able to read package labels is important
  • Overweight/obesity
  • Food and nutrition knowledge deficit
  • Physical inactivity
121
Q

Nutrition Therapy for Hypertension – Intervention

A

Comprehensive approach that addresses multiple lifestyle factors

◦ DASH: Dietary Approaches to Stop Hypertension

◦ Weight loss
◦ Sodium
◦ Alcohol

◦ Potassium, calcium, and magnesium ◦ Physical activity
◦ Smoking cessation

122
Q

Describe weight reduction as a Lifestyle Modification for Managing HTN

recommednation and approximate SBP reduction

A

recommendation: maintain normal body weigth (normal BMI)

approximate SBP reduction: 5-20 mm Hg/10 kg

123
Q

Describe DAH diet as a Lifestyle Modification for Managing HTN

recommednation and approximate SBP reduction

A

Consume a diet high in fruits, vegetables, low-fat diary products with reduced saturated fat and total fat

SBP reduciton:8-14 mm Hg

124
Q

Describe lower sodium intake diet as a Lifestyle Modification for Managing HTN

recommednation and approximate SBP reduction

A

1) consume no more than 2400 mg of sodium/day
2) further reduction of sodium intake to 1500 mg/day is desirable since it is associated with even greater reduciton in BP- especially in people wih REFRACTORY BP
3) reduce intake at least 1000mg/day since that will lower BP, even if the desired daily sodium intake is not achived

reduction in SBP: 2-8mm Hg

125
Q

Describe physical acitivity diet as a Lifestyle Modification for Managing HTN

recommednation and approximate SBP reduction

A

Engage in regular aerobic physical activity of at leasr 30 min per day, most days of the week

reduction in SBP: 4-9 mm Hg

126
Q
A
127
Q

Describe moderation of alochol consumption a Lifestyle Modification for Managing HTN

recommednation and approximate SBP reduction

A

limit to 2drink/day for man 3 drink for women

reduction in SBP: 2-4 mm Hg

128
Q

Can you combine Lifestyle Modifications techniques

A

yes, the more the factors, the bigger the impact

129
Q

Rationale of DASH

A
  • negative correlations between blood pressure and certain nutrients intake (potassium, calcium, magnesium, fibers and proteins)
  • this rationale came from observational studies
130
Q

What were the caracterisics of diets in the DASH diet study?

A

§ Control diet – western diet (poor in Ca, K and Mg)

§ Rich in vegetables and fruits diet (high in K, Mg and fibers)

§ Mixed diet - DASH diet, rich in vegetables and fruits, legumes and low-fat dairy (high in K, Mg, Ca, fibers, and poor in total fat, SFA and dietary cholesterol)

For all:

Sodium intake = 3 g for all diets
Weight-maintaining
Equal energy and fat content

131
Q

Benefits of the DASH diet as seen from the results of the study

A

§ Average ↓ 5.5 mmHg systolic BP and 3.0 mmHg diastolic BP more in DASH vs. Control

§ Further decrease in hypertensive subjects : ↓ 11.4 mm Hg/5.5 mmHg

§ ~ half of the DASH effects were observed for the high V&F diet vs. Control thus diets that are not only high in K, Mg and fibers, but also poor in total fat, SFA and dietary cholesterol are more beneficial for BP reduction )

132
Q

“AMDR” used in the DASH studies

A

55% CHO

18% protein

27% fat, including 6% saturated fat

133
Q

Bread, veggies, fruits, dairy, meat, nuts, oils signigiance to the DASH eatign pattern

A
134
Q

recommened itnake of different food groups for different calories (servings/day)

A
135
Q
A
136
Q

Benefits of low (1 500mg) Na diet combined with DASH diet

when is it recommended

A

→ greater combined effects on BP
-> recommended when refractory hypertension

137
Q

DASH vs mediterrannean

A

Largest effects in DASH vs Mediterranean diet

138
Q

When woudl 1500mg diet + DASH diet be recomended? what woudl be recommended in other cases?

A

1500 will be recommended only in refractory BP

in other cases regular DASH will be recommended which contains 2300 mg of Na

139
Q

Why wouldn’t you recommend 1500mg of Na

A

too hard to sustain

plus by just beign on DASH diet, there will already be a big decrease on BP

140
Q

what was the impact of DASH diet on SBP and DBP in the meta-analysis study

A

reduction of SBP by -7.62 mm Hg& DBP by -4.22 mm Hg

141
Q

OmniHeart study- describe

Results?

A

Conducted in prehypertensive or hypertensive adults

3 healthy diets similar to DASH-sodium, but with certain modifications:

  • rich in CHO
  • rich in protein (25% of E, 1:1 animal:plant sources vs 18% in DASH)
  • rich in unsaturated (mostly mono) fatty acids

Results:

→ All diets reduced blood pressure, LDL-C and cardiovascular risk (thus benefits in CV risk will be observed with other diets)

→ Diet high in protein and unsaturated fatty acids further decrease blood pressure in hypertensive individuals

142
Q

Comparison of control diet, typical DASH-diet and higher-fat/low CHO DASH diet,

WHat was the source of fat?

results?

A

higher fat dairy instead of low-fat that is usually consumed durign DASH

Higher-fat/low CHO DASH diet vs. DASH diet:

  • similar ↓ in blood pressure
  • ↓ triglycerides and large and medium VLDL particle concentrations
  • Did not ↓ LDL-cholesterol but ↑LDL peak particle diameter
143
Q

What are the components of DASH diet

A

increasing potassium, magnesium, calcium and fibers, while reducing saturated fatty acids and sodium, 2300mg of Na

144
Q

What does DASH improve?

A

blood pressure, LDL, VLDL and triglycerides

145
Q

When should drug treatment be prescribed

A
  1. average SBP ≥ 160 mmHg or DBP ≥ 100 mmHg

in patients without macrovascular target organ damage or other CVD risk factors.

  1. average SBP ≥ 140 mmHg or DBP ≥ 90 mmHg
    in the presence of macrovascular target organ damage or CVD risk factors. The above recommendations are regardless of age.
146
Q

Name 7 Antihypertensive drugs

A
  • Thiazide diuretics
  • Distal tubular diuretics
  • Angiotensin converting enzyme (ACE) inhibitors
  • Angiotensin II Receptor Blockers (ARB)
  • Calcium channel blockers (CCB)
  • Beta blockers
  • Single pill combination (SPC)
147
Q

Indications for drug treatment table

A
148
Q

What is SBP that is considered to be hight risK

A

≥ 130mmHg

149
Q

First line of treatment of adults with systolic/diastolic HTN without other compelling indications

A

individuals don’t have target organ damage and diabetes-> they are at low/moderate risk

Target: blood pressure of <140/90 mmHg

First line of treaatment: lifestyle modifications

There order of drugs listed is the order tof their addition to the treatment

ACEI: Angiotensin converting enzyme inhibitors; ARB: angiotensin II receptor blocker, CCB: Ca channel blockers

150
Q

What are the recommendations for SPC choices?

A

Recommended SPC choices are those in which an ACE-I is combined with a CCB, an ARB with a CCB, or an ACE-I or ARB with a diuretic

151
Q

What are the treatment goals for most (low/moderate risk), diabetes, hihg-risk

A

In most: SBP < 140 mmHg DBP < 90 mmHg

With diabetes (as they are higher up the scale-> the goal is lower): SBP < 130 mmHg DBP < 80 mmHg

With high-risks: SBP < 120 mmHg

152
Q

Drug Tx - possible Considerations

A

Location of the drug metabolism and excretion

Drug/ nutrient interactions

Drug / drug interactions

Nutritional status

153
Q

Drug Tx Considerations of location of drug metabolism and excretion:

A

if the organs that metabolize are affected by disease-> drug metabolism can be affected

e.g. liver and kidney

154
Q

Drug Tx Considerations of drug/nutrient interactions

A

◦ Drug-> nutrient metabolism, excretion or
◦ Nutrient-> drug metabolism, effect, excretion

◦ With all HTN drug Tx: avoid natural licorice (glycyrrhinic acid)

155
Q

Drug Tx Considerations of nutritional status

A

E.g. low albumin may increase drug effect because of more free drug in the blood

156
Q

Drug Tx consideration of physiological status

A

Pregnancy, lactation, presence of disease

157
Q

Drug Tx: Complicated HTN and diabetes

A

◦ With complications: ACEi or ARB (Angiotensin II receptor blockers)

◦ In absence of complications: ACEi or ARB or CCB or diuretics; these drugs protect the patient from further target organ damage

158
Q

Drug Tx: Complicated HTN adn coronary artery disease

A

◦ ACEi or ARB
◦ β-blockers or CCB for stable angina

159
Q

Drug Tx: Complicated HTN and Heart failure

A

◦ ACEi or ARB + β-blockers

160
Q

What are the 2 main Diuretic mechanisms and their characteristics?

A

Loop and thiazides

  • Decreased reabsorption of Na and K
  • Production of osmotic diuresis
  • Increased excretion of Na and K (and H+)

K-sparing:

  • Inhibit action of aldosterone-> no potassium losses
161
Q

Loop diuretics (K losing): generic name + side effects

A

furosemide

Side effects: hypokalemia, hyperglycemia, anorexia, N/V, constipation

162
Q

Thiazides (k loosing) generic name + side effects

A

◦ Side effets: hypokalemia, hyperglycemia, anorexia, malaise, muscle weakness

hydrochlorothiazide

163
Q

Nutritonalsupplements recommendations for both loop and thiazides:

A

◦ Provide potassium-rich foods

◦ Provide potassium supplements only when patient cannot consume sufficient amount of potassium in diet as they irritate mucosal lining, increased risk for ulceration, N/V/D

164
Q

Potassium Sparing: spironolactone (AldactoneTM), triamterene, amiloride- nutritional recommendations

A

◦ Avoid excess dietary potassium and supplements
◦ Avoid salt substitutes
◦ Avoid excess water consumption

◦ Take with food
◦ Avoid natural licorice

165
Q

Ace inhibitors- generic name + mechanism

A

Ramipril

inhibit conversion of angiotensin I to angiotensin II-> decrease vasoconstriction, vasopressin, inhibits aldosterone release

166
Q

Ace inhibitors side effects/interactions

A
  • hypotension (older patients), dry cough, may worsen renal function and hyperkalemia
  • side effects are increased in African Americans
  • avoid salt substitutes
  • avoid natural licorice
167
Q

Angiotensin II receptor blockers (ARB) general names + mechanism

When are these used?

A

valsartan, losartan

Usually used when ACEi are not tolerated (side effects)

Mechanism: block angiotensin II receptor and therefore decreases its activityàvasodilation, reduced vasopressin and aldosterone; similar result to ACEi but act on receptor instead of the conversion process

168
Q
A
169
Q

Angiotensin II receptor blockers (ARB) side effects/interactions

A

◦ Hyperkalemia, nausea, dizziness

◦ Avoid salt substitutes
◦ Avoid natural licorice
◦ Caution with grapefruit- competes with the drug in the liver for the metabolism

170
Q

Calcium channel blockers

generic name + mechanism

A

Amlodipine

affect the movement of Ca through Ca channels causing blood vessel relaxation (especially large vessels)

171
Q

Calcium channel blockers side effects/interactions

Contraindication

A
  • Edema, nausea, heartburn
  • Avoid natural licorice
  • Limit caffeine
  • Limit or avoid alcohol
  • Avoid grapefruit with felodipine (Plendil TM)

Contraindication: heart failure

172
Q

Beta-blockers

General name + mechanisms

A

Propanolol, atenolol, metoprolol
Mechanism: block adrenergic beta-receptors in the heart (B1)-> decrease rate and cardiac output

173
Q

Beta-blockers

side effects/interactions

Contraindications

A

Side effects/ interactions:

◦ N/V, constipation/diarrhea, bloating, masks symptoms of hypoglycemia (caution w/diabetes), dizziness, fatigue, CHF, hallucinations, insomnia

◦ Avoid natural licorice

Beta-blockers are not recommended as initial therapy in those over 60 years of age as they have a decreased adrenergic responsiveness, plus Beta-blockers are at the bottom of the list of medications-> a person will be takign a lot fo drugs

174
Q

Thresholds and targets FOR TREATMENT

A
175
Q

What is the effect of digitalis-like factor in hypertension?

A

Digitalis-like factor mediates sodium retention by increasing the activity and expression of the renal sodium pump-> increased sodium conservation

176
Q

When would we presribe HTN meds for 80+ and who do not have diabetes or target organ damage? Why?

A
  1. In the very elderly (aged ≥ 80 years) who do not have diabetes or target organ damage, the SBP threshold for initiating drug therapy is ≥ 160 mm Hg. This is due to the fact that as there are side effects of medications-> harder to handle those when you are older

NUTR 344 (22 decks)

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