Hypertension Flashcards

1
Q

major forms of CVD

A

hypertension, atherosclerosis, ischemic heart disease, peripheral vascular disease, heart failure, cerebrovascular disease

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2
Q

leading cause of death in canada

A

disease of the heart and cerebrovascular disease (24 % combined)

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3
Q

prevalence is ____________

A

going up in both males and females- more so in males

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4
Q

how many people are actually aware of their condition

A

65% treated and controlled, 18% unaware, 14% treated but not controlled, 4% aware, not treated

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5
Q

visits to the doctor

A

hypertension leading cause - by a lot!!

- more than diabetes

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6
Q

hypertension affects >__/5, what %?

A

more than 1 in 5 people, 22% Canadians over 20 , but since 18% not aware this number is actually much higher

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7
Q

the lifetime risk of developing hypertension in adults 55-65 with normal BP is?

A

90%

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8
Q

is hypertension the number one reason for taking medication?

A

yes

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9
Q

one in how many Americans have hypertension

A

one in 3

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10
Q

how is more at risk of hypertension

A

males, African-america, than whites, than hispanic, than Japanese, than Chinese

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11
Q

MAP

A

(mean arterial pressure) =
the average pressure in a patients arteries during one cardiac cycle. better indicator of the perfusion to vital organs than systolic bp.
found by:
cardiac output x peripheral resistance

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12
Q

cardiac output

A

= stoke volume x heart rate

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13
Q

peripheral resistance

A

= (length of vessel x viscosity of blood) / radius ^4

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14
Q

what 4 things regulate MAP?

A
  1. sympathetic NS
  2. RAAS
  3. renal function
  4. hormones
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15
Q

which hormones are involved in regulating MAP

A

epinephrine, vasopressin, angiotensin II

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16
Q

explain the big “factors influencing MAP” chart in you own words

A

the 2 factors influencing MAP are cardiac output and total peripheral resistance.

  • CO is determined by HR and stoke volume.
  • HR is determined by either PSNS or SNS/epinephrine. stroke volume is determined by SNS/epinephrine or venous return.
  • venous return is a big one. it is affected by blood volume (affected by vasopressin and angiotensin II, salt and water balance), respiratory activity, skeletal muscle activity and cardiac-suction effect.
  • on the other side, TPR is determined by arteriolar radius ( determined by skeletal muscle activity leading to local metabolic control, and SNS/epinephrine activity and vasopressin/ angiotensin leading to extrinsic vasoconstriction control) and by blood viscosity which is determined by # of RBC
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17
Q

primary HPT vs secondary

A

primary 95 % of cases- is idiopathic meaning that there is no known cause and secondary is caused by another issue/disease such s renal disease or CVD, endocrine disorders

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18
Q

causes of primary HPT

A

cause is not know! however many factors are at play –> individual differences in RAAS, in genes responsible for salt retention etc, in lifestyle choices ( stress, smoking, diet, excersise)

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19
Q

hypertensive individuals often secrete / overproduce?

A

vasopressin and angiotensin ( causes vasoconstriction and fluid retention)

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20
Q

non-modifiable risk factors of HPT

A

over 60, males, postmenopausal women, ethnicity, family history

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21
Q

modifiable risk factors

A

smoking, excersise, sodium intake, obesity, poor diet, stress

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22
Q

how does smoking contribute to HPT

A

interfere with NO–> impairs endothelial vasodilation

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23
Q

how does renal disease contribute to HPT

A

reduced blood flow, increased angiotensin, vasoconstriction and electrolyte/water retention, increases BV

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24
Q

is hyperinsulinemia associated with HPT

A

yes but mechanism is unclear

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25
Q

how would adrenal issues contribute to HPT

A

increase epinephrine and norepinephrine lead to vasoconstriction and increased cardiac output

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26
Q

how is HPT classified?

A

readings greater than 140/90 mm Hg (inclusive) are considered hypertensive. this does not mean that Bothe umbers have to be here, could be 140/80 and still hypertensive

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27
Q

why is hypertension a silent killer?

A

asymptomatic

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28
Q

what happens in response to low NaCl- / low ECF volume and low arterial blood pressure

A

the kidneys secrete renin, which converted circulating ( from the liver) angiotensinogen into angiotensin I, the lungs secrete converting enzyme to change 1 into 2, and angiotensin 2 acts on adrenal cortex to release aldosterone ( conserve Na+– passively water saved swell), and thirst is triggered and vasopressin release ( to reabsorb more water ( aquaporins) ) and acts on arteries to vasoconstriction –> all these in place to save body from harmful low BP

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29
Q

where is vasopressin released from

A

the posterior pituitary ( made in the hypothalamus)

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30
Q

what organs are affected by hypertension

A

brain - hemorrhage and stroke
kidney- renal failure and proteinuria
heart- CHD, CHF, LVH
eyes - retinopathy ( damage to the retina)
peripheral vascular disease ( blood circulation disorder)

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31
Q

what is top number reading

A

systolic

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32
Q

what is bottom number reading

A

diastolic

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33
Q

normal systolic

A

90-119

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34
Q

normal diastolic

A

60-79

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35
Q

stage 1 hypertensive

A

140-156/ 90-99

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36
Q

stage 2 HPT

A

160-179/ 100-109

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37
Q

stage 3

A

> 180/ >110

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38
Q

cerebrovascular diseases

A

diseases or conditions relating to blood supply to the brain –> stoke, dementia, hemorrhage

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39
Q

ACC stands for?

A

associated clinical conditions

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40
Q

list some ACC and target organ damage (TOD) that can occur from HPT

A
CVD - coronary artery disease, left ventricle hypertrophy, heart failure
cerebrovascular Diseases 
retinopathy
nephropathy
peripheral artery disease
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41
Q

TOD

A

TOD is the structural and functional impairment of major body organs due to elevated blood pressure (BP).

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42
Q

who is at high risk ?

A

one or more of the following:

  • clinical or sub-clinical CVD
  • chronic kidney disease
  • 10 year global cardiovascular risk >15%
  • above the age of 75
43
Q

who is at moderate to high risk

A

multiple CV risk factors and 10-year global risk >15%

44
Q

who is at low risk?

A

no TOD or cardiovascular risk factors

45
Q

why do we want to stratify risk ?

A

based on risk there are different thresholds and targets for treatment

46
Q

if high risk what BP treatment target are we aiming for?

A

<120 /NA diastolic

47
Q

if diabetic patient what BP target are we aiming for?

A

<130/ <80

48
Q

if moderate risk what target BP?

A

<140/ <90

49
Q

if low res what BP are we aiming for

A

<140 / <90

50
Q

how does the threshold for starting antihypertensive therapy change with the risk of patient

A

the higher the risk, the lower the BP reading to start treatment ( for example, if high risk and patient has BP reading of >130/ NA then we start antihypertensive therapy, but if patient is low risk than we wouldn’t Strat until patient is at reading of >160 /100

51
Q

how do we measure BP

A

automated office BP (AOBP)

oscillometric ( electric is preferred) vs non-automated office BP

52
Q

out of office BP measurements method

A

ambulatory - relating to or adapted for walking

53
Q

differences in reading for AOBP and non-AOBP

A

When using AOBP, a displayed mean SBP ≥135 mmHg or DBP ≥85 mmHg is high (Grade D). ii. When using non-AOBP, a mean systolic BP (SBP) ≥140 mmHg or diastolic BP (DBP) ≥90 mmHg is high,

54
Q

describe the path of diagnosing HPT

A

elevated BP reading -> go see doctor–> if mean office BP >180/110 - yup , if no AOBP is >135/85 or non-AOBP >140/80 then tell you to go home and need to take out of office measurements –> bc could be white coat hypertension –> at home if reading is > 135/85 with ABPM, then yes hyper tension, if no than white coat hypertension.

55
Q

how does diagnosis differ with diabetes?

A

if AOBP or non-AOBP reading is >130/80 then the patient need to take readings at home ( this is different bc for non-diabetic the range is 135/85

56
Q

goals of treatment

A
  • reduce the risk of CD and renal disease

- lower BP to clinically appropriate levels

57
Q

dietary constituents in HPT

A
high cal/weight/obesity
Na
K
Mg
Ca
alcohol
58
Q

___ % of under 55 yr old who have excess weight and a normal BP will develop HPT in the next 4 years

A

60% !! (direct link btw excess weight and HPT

59
Q

why is HPT related to obesity

A

insulin resistance/hyperinsulema
overactivity of the SNS
alterations in RAAS
leptin increases sympathetic activity–> function is preserved even in leptin resistance (meaning resistant to appetite control) individuals; still affects the SNS

60
Q

most beneficial non-pharm approach to HPT

A

weight loss, 10kg loss = 5-20 mmHG reduced

61
Q

10 kg loss =

A

5-20 mmHg

62
Q

all overweight patients should aim for a loss of ?

A

5kg to reduce BP

63
Q

weight loss could be difficult in patients with?

A

beta blockers- Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine

64
Q

what did high sodium intake do for patients with hypertension

A

increases risk of CHD death, CVD death and all death

65
Q

AI for sodium

A

1500 mg/day for 14-50 yr
1300 for 50-70
1200 for above 70

66
Q

UL for sodium

A

2300 mg/day for ALL

67
Q

average daily intake

A

3400 mg/day

68
Q

CHEP recommends

A

reduce sodium to 2000mg/day

69
Q

how much is 2000 mg of Na in salt?

A

5 g of salt which is just under a tsp

70
Q

major foods with sodium

A

breads, processed meats, soups, pasta, tomato dishes

71
Q

choose foods with less than ___ sodium

A

120 mg / serving or less than 5%

72
Q

3000 mg Na

A

no high Na processed foods and beverages

up to 0.25 tsp to cooking

73
Q

2000 mg Na diet

A

no high Na processed foods and beverages, no salt in prepration to foods, limit milk products to 2 cups/day

74
Q

1000 mg

A

same as 2000 but no canned, frozen, deli foods, cheese, margarine and no more than 2 servings of bread/day

75
Q

benefits of reducing sodium intake

A

found through epidemiological and ecological and intervention studies

  • reduce BP
  • prevent hypertension
  • additive effect with medications
  • reduces risk of complications
76
Q

potassium

A

inverse relationship between K and BP

- decreased prevalence of HPT with higher K intake

77
Q

potential mechanism of K intake

A
  • natriuresis
  • suppressed renin
  • vasodilation
  • reduce sympathetic activity and angiotensin II
78
Q

contributing factors for HPT

A

smoking (NO), excessive vasopressin, renal disease ( reduced blood flow will secrete more angiotensin II, adrenal disorders, hyperinsulinemia

79
Q

patients with HPT have an increased risk of TOD such as

A
heart-> CAD, LVH, HF
brain--> stroke, dementia
retinopathy
nephropathy
rest of body -peripheral artery disease
80
Q

describe hypertension Canada’s stratifying risk system

A

canada stratifies patients based on cardiovascular risk and then treatment is adjusted based on that risk ( so if a patient is high risk, the S/D threshold is going to be lower to administer medication than someone with hypertension but low risk) as well the BP treatment target is going to be LOWER - really want to minimize the risk

81
Q

high-risk patients

A

patients with one or more of the following clinical indications:

  • clinical or sub-clinical TOD such as CVD
  • Chronic kidney disease
  • age: over 75
  • estimated 10-year global cardiovascular risk > 15%
  • diabetes mellitus
82
Q

moderate to high risk patients

A

multiple CVD risk FACTORS and 10 year global risk greater than 15%

83
Q

low risk

A

no TOD or cardiovascular risk factors

84
Q

BP threshold for initiation of antihypertensive therapy for a high risk patient ?

A

greater than 130 SBP (same as if diabetic)

- want to aim for a treatment target of <120 for high risk and less than 130/80 for diabetic

85
Q

BP threshold for initiation of antihypertensive therapy for a moderate to high risk patient?

A

greater than 140 or greater than 90 - aim to be less than 140 and 90

86
Q

BP threshold for initiation of antihypertensive therapy for a low risk patient

A

greater than 160 or greater than 100 - aim to be less than 140 and 90

87
Q

dietary things to consider for HPT

A

Mg, Na, K, Ca, alcohol, excess calories,

88
Q

in adults over 55 what has been proven with weight and HPT

A

direct link excess weight and HPT–> 60% will develop in net 4 years
- caused from insulin res, overactive SNS (leptin activates), RAAS alterations

89
Q

what does leptin have to do with excess weight and HPT

A

leptin activates SNS and an over active SNS may need to HPT

90
Q

most potent no pharmacological approach

A

weight loss (5-15% loss has significant impact)

91
Q

all overweight patients should aim for?

A

weight loss of 5kg to drop SBP to 4.4 and DBP to 3.6mmHG)

92
Q

first line treatment ?

A

weight loss and PA and smoking cessation

93
Q

B-blockers

A

makes weight loss more challenging ( bc reduce heart weight, (think they block SNS epinephrine on heart ), and may cause weight gain

94
Q

what may affect salt responders/non-responders

A

age, severity of HPT, RAAS, potassium, genetics

95
Q

average sodium intake vs recommended

A

3.5g vs limit to 2000 mg (less than 1 tsp of salt)

ideally 1500mg

96
Q

potassium mechanism

A

surpress’s renin, naturens, vasodialation, reduce SNS

97
Q

Na/K ATPase in the kidney vs in smooth muscle / everywhere else cells

A

on the basolateral side of the tubual cells, Na+ is retained and K+ is excreted (think of aldosterone effect), whereas in every where else ( tears are salty) and 3Na is excreted and 2K+ is into cells

98
Q

excess Na and deficient K (LONG TERM) causes what in muscle cells, leading to impaired contraction and more peripheral resistance = increasing BP

A

excess Na INHIBITS the pump (normally, 3Na+ out and 2K+ in ), thus causing no Na out and more sodium retained in the cell. when this happens Na+/Ca+ transporter is activated. more Ca into cell! membrane voltage triggers! cause K+ to leave (depolarize), Ca+ triggers contraction! increase BP

99
Q

amount of K+ should be more than

A

2300 mg

not recommended to supplement- only if diuretic induced hypokalemia

100
Q

who is at risk of hypokalemia

A

RAAS inhibitors
other drugs
kidney disease

101
Q

calcium and Mg intake in relation to BP

A

inverse to BP

want moe to lower BP

102
Q

why calcium intake good to BP

A

more NA excretion, more sensitivity to NO, less vasoconstrictor production

103
Q

alcohol on BP

A

immediate lowering but then increases it next 10-15 hours ( dose-dependent)
- limit to 2 drinks men, 1 women