Monica - Week 9 - Exam 3 Flashcards

1
Q

what are three characteristics of hypertension?

A
  • damages arterial blood vessel
  • asymtomatic for years
  • risk factor for MI, CVA, HF, RF, PVD
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2
Q

____% of adults with HTN can be treated with _______ and also may require _____________

A

46; lifestyle changes; drug therapy

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3
Q

only _____% follow treatment

A

20

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4
Q

up to ___% fail to fill prescriptions

A

25

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5
Q

why do those people fail to fill prescriptions?

A
  • don’t want to believe it
  • think they don’t need it
  • feel fine (asymptomatic)
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6
Q

what are the 4 non-modifiable risk factors?

A
  • family history
  • age
  • gender
  • ethnicity
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7
Q

what is the percentage of HTN d/t genetics?

A

30 - 40; specific genes predispose to HTN

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8
Q

what occurs with age r/t HTN?

A

blood vessels lose elasticity with ↑ age

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9
Q

what are 3 characteristics of HTN r/t gender?

A
  • 56% of women and 59% of men
  • before middle ages, more common in males
  • age > 65 more common in females
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10
Q

what are 3 characteristics of HTN r/t ethnicity? Who is more sensitive?

A
  • African Americans more salt-sensitive
  • develop HTN at a younger age
  • need more aggressive therapy
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11
Q

why are African Americans more salt sensitive?

A

they have a gene that makes them more sensitive to salt

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12
Q

what are 6 modifiable risk factors of HTN?

A
  • lack of physical activity (obesity, ↑ strain on ♥, ↑ triglycerides, ↑ risk of diabetes)
  • dietary (↑ cholesterol, ↑ salt)
  • nicotine (↑ risk for damaged arteries)
  • stress- socioeconomic status
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13
Q

what is considered “normal” blood pressure?

A

SBP < 120 and DBP < 80

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14
Q

what is elevated blood pressure?

A

SBP 120 - 129 and DBP < 80

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15
Q

what is high blood pressure stage 1?

A

SBP 130 - 139 OR DBP 80 - 89

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16
Q

what is high blood pressure stage 2?

A

SBP 140 or higher OR DBP > 90

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17
Q

what is hypertensive crisis?

A

SBP > 180 and/or DBP > 120

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18
Q

what is the percentage of primary hypertension?

A

90 - 95% of cases

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19
Q

what is primary hypertension?

A

BP ↑ without identified cause

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20
Q

what are the contributing factors to primary hypertension?

A

↑ Na intake, ↑ BMI, DM, Smoking, Excessive alcohol intake, hyperaldosteronism, family history

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21
Q

what is the percentage of secondary hypertension?

A

5 - 10 % of cases

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22
Q

what is secondary hypertension? An example?

A

underlying cause can be identified and corrected. Ex. HTN pregnancy .

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23
Q

what is a complication of HTN?

A

target-organ damage

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24
Q

what systems are affected in target organ damage?

A

heart, brain, peripheral vascular disease, nephrosclerosis, and retinal damage.

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25
which specific disease are caused d/t heart target organ damage?
- coronary artery disease | - left ventricular hypertrophy
26
what occurs during target organ damage of the brain?
plaque formation in carotid arteries → TIA o? r stroke
27
what occurs during target organ damage r/t peripheral vascular disease?
intermittent claudation (s/sx) → ischemic leg pain with activity (rest = no pain)
28
what occurs during nephrosclerosis?
atrophy of tubules and destruction of glomeruli = ↓ kidney function
29
what occurs during retinal damage?
blurred vision and vision loss
30
what can occur with athrosclerosis?
hemorrhage
31
what is the process map of short term mechanism regulation of BP for DECREASED BP?
- baroreceptors sense a ↓ BP - SNS is activated - ↑ HR, ↑ cardiac contractility, vasocontriction
32
what is the process map of short term mechanismm regulation of BP for INCREASE BP?
- baroreceptors sense a ↑ BP - inhibitor signals go to brain stem - ↓ HR, ↓ force of contraction, vasodilation
33
what occurs to baroreceptors with those with HTN?
overtime baroreceptors recognize ↑ BP as "normal"
34
what is the long term regulation of BP?
RAAS (renin-angiotensin-aldosterone systems)
35
what 3 things occur during RAAS?
- Na+ and H2O retention - ↑ ECF volume - vasoconstriction of the arteries
36
what things occur with the long term presence of angiotensin II?
- hypertrophy of the myocardial cells (causes enlarge ♥) - collagen deposits (scar-like tissues) - cardiac remodeling (↑ risk of morbid/mortal of ♥ failure) - accelerates deposition of fatty plagues - ↑ risk of MI and CVA
37
what are 4 first line hypertension agents?
- thiazide diuretics - calcium-channel blockers - angiotensin-converting enzyme (ACE) inhibitors - angiotensin- receptor blockers (ARBs)
38
what are 5 second line hypertension agents?
- diuretics - beta-blockers - alpha-blockers - centrally alpha-agonists - direct vasodilators
39
what is the drug for ACE inhibitors?
lisinopril - there are 10 in this category that end in "pril"
40
how does lisinopril work? (5 mechanisms)
- inhibits conversion of Angio I → Angio II - ↓ systemic vascular resistance - ↓ aldosterone secretion (no Na+/H2O retention/retention of K+) - slows down progression of cardiac remodeling - reduces glomerular filtration pressure ("renoprotective/cardioprotective")
41
what are the AE of lisinopril?
dry cough, ED, orthostatic hypotension, possible hyperkalemia
42
what are special considerations for lisinopril?
metabolized and excreted by kidneys → dose adjustments for renal impairment
43
what is the drug for angiotensin II receptor blockers?
losartan - there are 8 drugs in this category that end in "tan"
44
how does losartan work? (3 mechanisms)
- blocks Ag II receptors in arterioles (no vasoconstrict) - block Ag II receptors in adrenal gland (no aldost/no absorption of Na+/H2O) - blocks Ag II receptors in heart (prevent ♥ remodeling)
45
losartan is used in _________ __________
diabetic nephropathy
46
what are the AEs of losartan?
hypotension, hyperkalemia, and hypoglycemia | ***DOESNT PRODUCE DRY COUGH
47
what are special considerations for losartan?
- doses are adjusted for kidney pts | - be aware of K+ sparing products/supplements
48
what is the main alpha-1 blocker drug?
doxazosin
49
where does doxazosin work?
- alpha 1 receptors located in arterial and venous smooth muscle, GI, GU - blocks alpha-1 receptor from binding with norepinephrine
50
how does doxazosin work? (3 mechanisms)
- alpha-1 activation —> vasoconstriction - blocking alpha-1 receptors in post-synapse —> decreased peripheral resistance and BP - prevents contractions of bladder neck and urethra (urine flow—>BPH)
51
what are the AEs of doxazosin?
dizziness, HA, decreased libido, and sexual dysfunction (noncompliance occurs d/g this) - first does orthostatic hypotension within first 24 hours; recommend take first dose at bed time to minimize chance of OH—> dizzy, fainting, syncope
52
what is the main drug of alpha-2 agonist?
clonidine
53
how does clonidine work?
- CNA action to decrease sympathetic activity | - lack of norepinephrine production —> reduced BO
54
what are the AEs with clonidine?
dry mouth, drowsiness, withdrawal phenomenon
55
what occurs to when clonidine is discontinued abruptly?
rebound hypertension - increased BP more than it was at patient’s baseline
56
clonidine is used as treatment for _____ ________
resistant HTN - when other first line drugs aren’t working
57
what is the main drug of vasodilators?
hydralazine
58
when is hydralazine used?
for moderate to severe HTN with diuretic - usually PRN IV form
59
how does hydralazine work? (2 mechanisms)
- dilate blood vessels - relax arteriolar smooth muscle which reduces peripheral resistance causing a hypotension effect (compensate by beating faster)
60
what is the AE of hydralazine?
tachycardia | other possible: edema, orthostatic hypotension
61
what are the 8 collaborative care and lifestyle modifications that can be made?
- Diet: DASH (Dietary Approach to Stop HTN) - decreasing Na+ intake (<2300 mg/day, ideal 1500mg/day; decrease by 1000mg/day) - weight reduction (ideal weight) - increase physical activity (90-150mins/week) - alcohol moderation (2 for men, 1 for women) - avoid tobacco products (nicotine= vasoconstriction) - psychosocial factors _ compliance with drug therapy
62
T/F: HTN has no cure, has to be managed. If you change your lifestyle, no need for pharmacotherapy
TRUE