8. Hypertension 1 Flashcards

1
Q

What are the major forms of CVD?

A
  • hypertension
  • atherosclerosis
  • ischemic heart disease
  • peripheral vascular disease
  • heart failure
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2
Q

CVD and heart diseases are one the leading causes of death in Canada (2018) in both men and women, behind which other cause of death?

A

Cancer

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3
Q

Typically, ______ have a higher prevalence of hypertension than _____. This prevalence flips as the population gets older (65+).

A
  • men
  • women
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4
Q

Hypertension affects _____ of Canadian adults aged 20+. ___% are not aware of their condition, so this number is probably undercutting the actual amount.

The lifetime risk of developing hypertension among adults aged 55-65 with normal blood pressure is _____%.

A
  • >1/5
  • 18%
  • 90%
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5
Q

What is the number one reason to visit a doctor and take medication?

A

Hypertension

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6
Q

Rates of hypertension vary by age, gender, and race/ethnicity. Which race shows the highest prevalence for hypertension? Which shows the least?

A
  • African-Americans
  • Chinese, Korean
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7
Q

What are the two phases of the cardiac cycle?

A

Systolic (contraction) and Diastolic (resting)

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8
Q

How do you calculate the MAP (mean arterial pressure)?

A

Cardiac output x Peripheral resistance

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9
Q

How can you calculate cardiac output (CO)?

A

CO= stroke volume x heart rate

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10
Q

How do you calculate peripheral resistance in the arteries?

A

( Length of vessel x viscosity of blood) / radius4

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11
Q

Why is the radius of the arteries important?

A

Even a tiny shift in radius will have a drastic effect on total resistance (radius4)

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12
Q

What is the effect of vasodilation on resistance?

A

Less resistance

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13
Q

What is the effect of vasoconstriction on resistance?

A

Resistance is increased

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14
Q

What systems and hormones are involved in blood pressure regulation?

A
  • sympathetic nervous system
  • renin-angiotensin-aldosterone system
  • renal function
  • Hormones: epinephrine, vasopressin, angiotensin II
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15
Q

Vasopressin increases the H20 reabsorption by the kidneys. This works alongside thirst signals that increase fluid intake and angiotensin II causing increased vasoconstriction to correct what changes to the system?

A
  • Low [NaCl]
  • Low ECF volume
  • Low arterial blood pressure
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16
Q

The brain, eyes, vascular system, heart, and kidneys are at risk of developing what problems when hypertension goes untreated over a long period of time?

A
  • brain: hemorrhage, stroke, dementia
  • eye: retinopathy
  • vascular: peripheral vascular disease
  • heart: LVH, CHD, CHF
  • kidney: renal failure, proteinuria
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17
Q

What do the following heart-disease acronyms stand for?

  • LVH
  • CHD
  • CHF
A
  • LVH: left ventricular hypertrophy
  • CHD: coronary heart disease
  • CHF: congestive heart failure
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18
Q

How is blood pressure manually measured?

A

By a trained professional using a sphygmomanometer; read in mmHg.

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19
Q

Why aren’t the terms benign and malignant used anymore when discussing hypertension?

A

Too often confused with cancer

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20
Q

There are two classifications of hypertension causes; Primary/essential and secondary.

What are the primary causes (make up 95% of hypertension cases) and what are the secondary causes (make up 5%)?

A

Primary:

  • unknown etiology
  • interaction from environment and genetics factors
  • influenced by dietary and behavioral factors

Secondary:

  • occurs as effect of renal, endocrine, or neurological disorders
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21
Q

Why is hypertension considered the “silent killer”?

A

It is typically asymptomatic

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22
Q

What are non-modifiable major risk factors of HTN?

A
  • > 60 y.o.
  • family history of CVD (women < 65 y.o., men < 55 y.o.)
  • men, postmenopausal women, ethnicity (af. american, russians, finns)
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23
Q

Why do pre-menopausal women show a lower prevalence of HTN versus men and post-menopausal women?

A

Estrogen appears to have a protective effect over HTN

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24
Q

What are major risks for HTN that are modifiable?

A
  • SMOKING
  • sedentary lifestyle
  • abdominal obesity
  • insulin resistance
  • excess sodium intake
  • poor diet quality
  • stress
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25
Q

How does excessive secretion of vasopressin and angiotensin II contribute to HTN?

A
  • high vasoconstriction and fluid retention
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26
Q

How does smoking contribute to HTN?

A
  • interferes with NO production
  • impairs endothelial vasodilation
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27
Q

How does renal disease contribute to HTN?

A
  • reduced blood flow leads to increased angiotensin II
  • vasoconstriction occurs, and a retention of Na+, Cl-, and water
  • Increased blood volume
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28
Q

How do adrenal disorders contribute to HTN?

A
  • increased secretion of epinephrine and norepinephrine
  • cause vasoconstriction and higher cardiac output
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29
Q

Neurological diseases and hyperinsulinemia is associated with HTN. How?

A

Unclear mechanisms for now.

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30
Q

In Canada, what patient with what disease is immediately considered a High-risk HTN patient?

A

If they have Diabetes Mellitus

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31
Q

Individuals over 50y with a SBP of 130-189 mmHg and one or more CV risk factors are considered at what risk for HTN?

Name a few potential CV risk factors.

A
  • Considered at High-Risk for HTN

CV Risk Factors:

  • clinical or sub-clinical cardiovascular disease
  • chronic kidney disease (nephropathy, proteinuria)
  • estimated 10-year global CV risk >15%
  • age > 75 y.o.
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32
Q

What is considered at moderate-to-high risk of HTN?

What about low risk?

A

Mod-to-High:

  • multiple CV risk factors
  • AND 10-year global risk 10-14%

Low:

  • no target organ damage or CV risk factors
  • 10-year global risk <10%
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33
Q

When treating a high-risk HTN patient in Canada, what is the target SBP to lower the risk as much as possible?

At what SBP is treatment usually started for those with a high-risk for HTN?

A
  • Medication to reduce SBP to <120 mmHg
  • >130 mmHg
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34
Q

What is the preferred method of measuring blood pressure in office? Why?

What is a downside of this measurement?

A
  • Automated office blood pressure (AOBP) or oscillometric (electronic)
  • It is done by the patient themselves (doesn’t require trained professional) and limits potential stressful influences on BP (doctor taking measurement and clinical setting can increase stress)
  • Limited to BP measurement in the moment
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35
Q

What is the best method for BP measurement out of office? Why?

A
  • Ambulatory blood pressure measurement (ABPM)
  • Outside the office (no stressors influencing BP) and measures over a longer period of time (better representation of BP)
36
Q

When are out-of-office BP measurements taken?

What mean office BP measurement diagnoses a patient as hypertensive?

A
  • When AOBP >135/85 mmHg OR the patient has diabetes
  • BP >180/110
37
Q

Out-of-office measurements are taken rule out what possibility when checking for HTN?

A

WCH (white coat hypertension)

  • elevated BP caused by clinical setting influence
38
Q

What are the main goals of HTN therapy?

A
  • lower BP to clinically appropriate level
  • Reduce risk of CVD and renal disease
39
Q

What is the basis of comprehensive HTN therapy plans?

When these methods aren’t sufficient, what else is added to the plan?

A

Basis:

  • physical activity
  • weight reduction (if necessary)
  • nutrition therapy
  • moderation of alcohol and smoking cessation
  • relaxing therapy

If not enough:

  • pharmacological interventions
40
Q

Loop diuretics, thiazides, carbonic anhydrase inhibitors and potassium sparing diuretics are all forms of what?

A

Pharmacological interventions used to treat HTN when the basic comprehensive plan isn’t sufficient.

41
Q

What are the dietary factors involved in hypertension?

A
  • high calories, excessive weight, obesity
  • sodium
  • potassium
  • calcium
  • magnesium
  • alcohol
42
Q

In adults < 55 y.o, there is a direct link between excess weight and HTN (60% will develop HTN in next 4 years). Abdominal obesity is more associated with HTN.

What are the causes of HTN associated with obesity?

A
  • insulin resistance/hyperinsulinemia
  • overactivity of the sympathetic nervous system (due to Leptin production and resistance)
  • alterations in RAAS (increased production of aldosterone)
43
Q

Increased leptin levels increase sympathetic activity, which is linked to HTN in patients suffering from obesity. How are leptin levels associated with weight?

A

Higher amounts of leptin are produced with higher amounts of fat mass.

44
Q

What is the most beneficial and effective method of reducing BP (not pharmacological) and preventing HTN?

Explain

A
  • Weight loss
  • BP shown to be reduced by 5-20 mmHg per 10kg lost
45
Q

When an overweight patient achieves a weight loss of 5 kg, what is the corresponding change in BP and risks for organ damage?

A
  • Lowers SBP by 4.4 mmHg
  • Lowers DPB by 3.6 mmHg

This is CLINICALLY RELEVANT and is shown to reduce BP and lower risks for organ damage.

46
Q

Weight loss may be more difficult for patients on beta-blockers for cardiac diseases. Why?

A
  • Sympathetic activity is lowered
  • Lower metabolic activity
47
Q

How is sodium intake measured?

A

Excretion of sodium is the most precise way of measuring sodium intake.

48
Q

For every increase of 100 mmol Na/day, what is the increase in BP?

A
  • SBP increased by 3-6
  • DBP increased by 0-3
49
Q

High _____ intake increases the risk of complications (CHD death, CVD death, and all death) in HTN patients.

A

Sodium

50
Q

What type of dietary treatment is recommended for patients with HTN?

A

DASH diet

51
Q

What can be seen in studies comparing the DASH diet SBPs and typical US diet SBPs at high, medium, and low levels of sodium intake?

A
  • Major benefits to SBP occur when going from medium to low levels of Na intake
  • Still beneficial to go from high to low levels of Na
  • DASH diet followers have lower SBP, regardless of Na intakes (lower than low-intake US typical dieters)
52
Q

⅓ of the population are not salt-sensitive, aka “non-responders”. What does this mean for SBP when changing levels of Na in the diet?

A

No change in SBP from different Na intakes.

53
Q

Salt sensitivity is largely influenced by…

A

Potassium

  • Higher K intake is associated with lower Na sensitivity
54
Q

What is the adequate intake of Na for adults 14-50 yo?

For adults 51-70 y.o.?

What is the UL?

A
  • 1500 mg/day
  • 1300 mg/day
  • 2300 mg/day
55
Q

What is the average total daily intake of sodium by Canadian adults?

Is this above or below the UL?

A
  • 3400 mg/day
  • Above: UL is 2300 mg/day
56
Q

____ tsp of salt has about 1,150 mg Na.

A

½ tsp

57
Q

What does the CHEP recommend for daily sodium intake to lower BP?

A

Reducing sodium intake towards 2,000 mg/day (5 g of salt)

58
Q

Where does 80% of the average sodium intake come from?

A

Processed foods

59
Q

Breads and other baked goods are one of the highest contributors to daily sodium intake and contribute more than cheese, soups, and even processed meats.

Why is this so?

A

Despite being lower in sodium content than other foods, the rate of consumption of breads and baked goods is higher than the others items. This accumulates greater amounts of daily sodium intake.

60
Q

What is recommended to be done when choosing foods to lower sodium intake?

A
  • Read nutrition labels: unsalted, lower sodium
  • Check serving sizes and note sodium amounts
  • Choose foods with less than 120 mg/serving or DV of <5%
61
Q

Diets restricting sodium at levels lower than 1000 mg/day are not usually recommended. Why?

A
  • Aren’t very pleasant and difficult to sustain
  • Very little benefits are shown when reducing below 1000 mg; not worth the unpleasantness
62
Q

When are sodium controlled diets prescribed?

A

For patients with renal diseases or HTN

63
Q

Reducing sodium intake has an additive effect to antihypertensive medications. Why?

A

Lowering Na intakes will lower the dosages of medication needed for control of HTN

64
Q

Despite the variability of responses to changes in sodium intake (non-responders), reducing sodium supply in processed foods is a ______ ______ ______.

Why?

A
  • Public health measure
  • ⅔ of population show improvements with reduced Na intakes
  • Low processed-food diets are typically very low in sodium content
65
Q

There is a(n) _______ relationship between potassium intake and BP.

A

inverse

  • Higher K = lower BP
66
Q

There is _______ prevalence of HTN with higher K intakes.

A

Decreased

67
Q

The effect of K on BP is inter-dependent with sodium.

Explain.

A
  • greater the increase of BP with Na, the greater the decrease with supplemental K
68
Q

K intake protects against _____ ________ of BP.

A

familial susceptibility

69
Q

What are the possible mechanisms of K effects on blood pressure?

A
  • Natriuresis (Na excretion in urine)
  • Suppressed renin
  • Reduces vascular contraction
  • May reduce sympathetic activity and angiotensin
70
Q

Higher sodium intakes are linked with _______ excretion of potassium.

A

increased

71
Q

The modern western diet is characterized by being high in sodium and low in potassium. How does this contribute to HTN prevalence?

A

High sodium intake:

  • retention of Na in kidneys
  • causes increased K excretion
  • Excess Na in body- increased ECF volume, excess Na in cells
  • Vascular contraction

Low potassium intake:

  • ineffective K-conservation
  • excessive renal/fecal K loss
  • K deficit in body (causes Na retention) and in cells
  • Vascular contraction

Vascular constriction

  • increases peripheral resistance —– HTN
72
Q

What effect does increased Na and decreased K have in the kidneys in primary HTN?

A
  • Increased angiotensin II and sympathetic activity in the proximal tubule leads to Na being reabsorbed through the luminal membrane of the renal tubular cell (via NHE-3 antiporter)
  • The build up of Na in the renal tubular cells influences the Na/K ATPase pump to favor the reabsorption of Na into the capillaries (through the basolateral membrane of the renal tubular cells) and the excretion of K
73
Q

How does the distal tubule influence the Na content of the renal tubular cells in primary hypertension?

A

Aldosterone levels stimulate the uptake of Na and the excretion of Cl through the NC cotransporter in the luminal membrane of the renal tubular cells.

74
Q

How are the collecting ducts involved in Na reabsorption into the renal tubular cells?

A

Aldosterone levels caused the transport of Na through the luminal membrane into the renal tubular cells via ENaC

75
Q

How is vascular contraction stimulated when Na intakes are high and K intakes are low?

A
  • Na/K ATPase pump is slightly inhibited, leading to a build up of Na+ in smooth muscle cells
  • Ca uptake is encouraged, depolarizing the membrane voltage
  • Ca channels are opened in the SR; favors action of actin and myosin
  • MUSCLE CONTRACTION
76
Q

On average, are Canadians meeting the daily recommended intakes of K: 2600 mg/day for women, 3400 mg/day in men?

A

Levels are pretty well met:

  • 2800 for women
  • 3300 for men
77
Q

Daily dietary intakes of K over 2300 mg is associated with deceased risk of:

A

Stroke mortality

78
Q

K supplementation for normotensive people ______ (is/is not) recommended as a way of preventing high BP.

K supplementation above daily dietary intake ______ (is/is not) recommended as a treatment for HT.

CFG recommends that potassium levels be met by __________.

A
  • is not
  • is not
  • Dietary means: fruits and veggies allow for sufficient K intake
79
Q

What is useful when someone has diuretic-induced hypokalemia?

A

Potassium supplements

80
Q

What are risk factors for hyperkalemia?

A
  • renin-angiotensin-aldosterone inhibitors
  • drugs causing hyperkalemia
  • chronic kidney disease
  • baseline serum K > 4.5 mmol/L
81
Q

Calcium intake is _____ associated with BP.

What are possible mechanisms explaining this relationship when calcium intake is high?

A

Inversely

  • higher sodium excretion
  • increased sensitivity to NO (vasodilation)
  • reduced production of vasoconstrictors (superoxyde and prostanoids)
82
Q

Is Ca supplementation above the RDI recommended as a means of preventing high BP?

Is Ca supplementation above DRI recommended as a treatment for HTN?

What is recommended regarded Ca intake?

A
  • No
  • No
  • CFG recommends consuming 2-3 portions of milk products daily as sufficient means of Ca intake
83
Q

Magnesium intake has a(n) _________ relationship with BP.

What is the potential mechanism involved?

Are supplements above DRI recommended?

A
  • inverse
  • relate to role of Mg in vascular structure and function (regulates vascular reactivity and contractility)
  • No
84
Q

Alcohol has a(n) __________ relationship with intake over 2/drinks per day and BP.

A

dose-response

85
Q

What is the immediate effect on BP with alcohol intake?

What happens afterwards and lasts for the next 10-15h?

What has moderate alcohol consumption been associated with?

A
  • Immediate vasovagal effect
  • Elevated BP for next 10-15h
  • Cardioprotective effects, doesn’t raise BP
86
Q

What mechanisms are proposed for alcohol and it’s effect on BP?

A
  • stimulates sympathetic nervous system
  • stimulates cortisol secretion
  • increases Ca uptake by cell membranes
87
Q

What are the recommended limits for alcohol consumption in men and women per day?

A
  • Men: 2 drinks per day
  • Women: 1 drink per day