hypertension Flashcards

1
Q

What are the two types of HTN?

A

primary(essential)
secondary

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2
Q

What does HTN being secondary mean?

A

it is caused by something

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3
Q

What can secondary HTN be caused by?

A

obstructive sleep apnea, renal impairment, diet, certain meds, etc.

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4
Q

HTN causes ___________ injury leading to impaired synthesis & release of ______ _________

A

endothelial; nitric oxide

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5
Q

What does HTN promote?

A

inflammatory mediators

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6
Q

What disease process does HTN accelerate?

A

the development of artherosclerosis

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7
Q

____ of the population over 18 have HTN

A

45%

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8
Q

What causes increased cardiac afterload & ventricular hypertrophy?

A

HTN

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9
Q

If HTN is left untreated it can lead to end-stage organ damage affecting what organs?

A

heart
brain
kidneys
arteries
eyes

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10
Q

What are the 7 players involved in HTN?

A

Norepinephrine
epinephrine
angiotensin II
histamine
serotonin
bradykinin
prostoglandin

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11
Q

What hormone is a strong vasoconstrictor?

A

norepinephrine

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12
Q

What is epinephrine a part of?

A

SNS stimulation

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13
Q

stimulation of the SNS during stress or exercise causes ______ constriction of veins & arterioles because of the release of _____________ from sympathetic nerve endings

A

local; norepinephrine

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14
Q

What does sympathetic stimulation cause the adrenal medulla to secrete?

A

norepinephrine & epinephrine

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15
Q

What does angiotensin II act as?

A

a very strong vasoconstrictor from RAAS

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16
Q

angiotensin II increases what?

A

BP

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17
Q

what effect does histamine have on arterioles?

A

vasodilator

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18
Q

What is serotonin released by?

A

the platelets

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19
Q

What does serotonin do?

A

causes vasoconstriction & can cause vascular spasm

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20
Q

What does bradykinin cause?

A
  • intense dilation of arterioles
  • increased capillary permeability
  • constriction of venules
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21
Q

What does bradykinin play a special role in?

A
  • regulating blood flow & capillary Leakage in inflamed tissues
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22
Q

What does bradykinin help regulate?

A

blood flow in the skin as well in the salivary & GI tract

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23
Q

What are prostaglandins made from?

A

arachidonic acid

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24
Q

What does tissue injury cause the release of?

A

arachidonic acid from the cell membrane, which initiates prostaglandin synthesis

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25
Q

What does prostaglandin cause?

A

some prostaglandins cause vasoconstriction & others cause vasodilation

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26
Q

What do corticosteroids do?

A

produce anti-inflammatory response by blocking release of arachidonic acid & preventing prostaglandin synthesis

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27
Q

What is BP?

A

cardiac output x arteriole resistance

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28
Q

What is first-ine treatment for HTN?

A

non-pharmacologic interventions
- diet
- exercise
- life-style management

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29
Q

What patient education should be focused on during the first-line tx?

A

diet
exercise
lifestyle management
- quality sleep
- smoking cessation
- alcohol consumption

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30
Q

What are first-line medication tx for HTN?

A
  • ACE inhibitors
  • ARBs
  • thiazide diuretics`
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31
Q

What type of medication is not really a first-line tx?

A

beta blockers

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32
Q

What should we do if BP goal is not met?

A
  • increased med dose
  • add second or third drug
  • change to a different drug
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33
Q

What does pharmacologic management of HTN do?

A

works to alter the body regulatory mechanisms

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34
Q

Are HTN medications a cure to HTN?

A

NO; they are a band-aid

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35
Q

What must you take into account when picking a medication for HTN?

A

comorbid diseases

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36
Q

Why may those with HTN need more than one medication to treat HTN?

A
  • to avoid maxing out the dose
  • to minimize/ avoid side effects
  • synergistic effect
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37
Q

What are the 6 classes of medications used to treat HTN?

A
  • ACE inhibitors
  • ARBs (angiotensin II receptor blockers
  • thiazide diuretics
  • beta blockers
  • calcium channel blockers
  • renin inhibitors
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38
Q

What are medications that are ACE inhibitors?

A

lisinopril
enalapril
ramipril

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39
Q

What are medications that are ARBs?

A

losartan
irbesartan
valsartan

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40
Q

What are medications that are thiazide diuretics?

A

hydrochlorothiazide (HCTZ)
chlorthalidone

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41
Q

What are medications that are beta blockers?

A

metoprolol
atenolol
bisoprolol
labetalol

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42
Q

What are medications that are calcium channel blockers?

A

amlodipine
felodipine
diltiazem
verapamil

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43
Q

What medication is a renin inhibitor?

A

aliskiren (tekturna)

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44
Q

Are renin inhibitors frequently used?

A

no; they are rarely used

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45
Q

How do thiazide diuretics work?

A
  • inhibit reabsorption of sodium & chloride from the distal tubules in the kidneys
  • decrease peripheral resistance
  • decrease preload
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46
Q

What are thiazide diuretics better for?

A

sodium sensitive HTN as in african americans & older adults

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47
Q

Are thiazide diuretics tolerated?

A

yes; generally well tolerated

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48
Q

What are the adverse effects of thiazide diuretics?

A
  • hypokalemia
  • hyperglycemia
  • gout exacerbation
  • other electrolyte imbalances (calcium)
  • orthostasis (orthostatic hypotension)
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49
Q

Should patients with a hx of gout be given thiazide diuretics?

A

no

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50
Q

why do thiazide diuretics cause gout exacerbations?

A

they increase uric acid

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51
Q

What are contraindications for thiazide diuretics?

A

sulfa allergy
renal impairment/ failure

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52
Q

What are the nursing considerations for thiazide diuretics?

A
  • increased risk of digoxin toxicity
  • decrease effectiveness of DM meds
  • increased risk of lithium toxicity
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53
Q

When should a thiazide diuretic be given?

A

early in the morning

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54
Q

What labs should be watched with a pt on thiazide diuretics?

A

potassium & glucose

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55
Q

What vitals should be monitored with a pt on thiazide diuretics?

A

BP & HR

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56
Q

What patient education should be given to a pt on a thiazide diuretics?

A

watch diet - be very clear
exercise
minimize alcohol
stop smoking
avoid NSAID (increase BP)

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57
Q

What are indications for angiotensin-converting enzymes (ACE) inhibitors?

A
  • HTN
  • heart failure
  • diabetes
  • post MI & PCI
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58
Q

What is the route of administration for most ACE inhibitors?

A

PO
enalapril can be given IV

59
Q

How do ACE inhibitors work?

A
  • decrease aldosterone production
  • inhibit angiotensin II production
  • decrease vasoconstriction
  • interferes with RAAS
  • keep the vasodilation effects of bradykinin
  • increase preload & afterload
60
Q

Are ACE inhibitors usually tolerated?

A

yes; generally well tolerated and absorbed

61
Q

What are adverse effects of ACE inhibitors?

A

hyperkalemia
dizziness
cough
angioedema

62
Q

Why do ACE inhibitors cause a dry cough?

A

related to kinins & activation of arachidonic pathway & prostaglandin production

63
Q

When does the cough usually begin once you have started an ACEI?

A

begins within 1 to 2 weeks of initiation

64
Q

When does the ACEI cough typically stop once discontinuing the medication?

A

typically resolves within a few days of stopping medication

65
Q

With what ethnic group do ACEI have an increased incidence/ worsened cough?

A

Chinese people

66
Q

Why does angioedema happen when taking an ACEI?

A
  • occurs because of elevated bradykinin causing vasodilation
  • angiotensin II responsible for inactivating bradykinin
67
Q

How often does angioedema occur with ACEI ?

A

rare & usually not causing any real harm; just looks bad

68
Q

What is the blackbox warning for ACEI?

A
  • serious fetal abnormalities; not given to women in pregnancy & use cautiously in childbearing women
  • contraception very important
69
Q

Why should ACEI not be given in the 3rd trimester of pregnancy?

A

it dries up amniotic fluid

70
Q

What are the nursing considerations for taking ACEI?

A
  • be aware of renal function & potassium
  • assess for orthostatic hypotension
  • awareness of administration to childbearing women
  • know when to hold
71
Q

What class of medications should not be taken with ACEI?

72
Q

Should ACEI be taken with or without food?

A

should be taken on an empty stomach

73
Q

What are the indications for angiotensin II receptor blockers (ARBs)?

A
  • hypertension
  • when an ACEI cannot be used
74
Q

How do angiotensin II receptor blockers (ARBs) work?

A
  • bind with AG-II receptors in vascular smooth muscle & adrenal cortex to stop vasoconstriction & aldosterone production
  • blocks AG-II from binding at the receptor sites in the brain, kidneys, heart, periphery & adrenal tissue
75
Q

What are the adverse effects of ARBs?

A
  • cough
  • hyperkalemia
  • headaches
  • dizziness & syncope
  • GI complaints
  • xerostomia (dry mouth)
  • alopecia
76
Q

Is the cough with ARBs more or less than with ACEI?

77
Q

Is the hyperkalemia with ARBs more or less than with ACEI?

78
Q

When taking ARBs there is an ________ in creatinine due to possible ________ glomerular filtration rate (GFR)

A

increase; decreased

79
Q

What should ARBs never be given with?

A

ACE inhibitors

80
Q

What are drug interactions with ARBs?

A

diltiazem & oral anti-fungals

81
Q

Are ARBs safe for pregnancy?

A

no; should be avoided during pregnancy

82
Q

What are nursing considerations for ARBs?

A
  • monitor renal function
  • some drug interactions related to cytochrome P450
  • can be given with or without food
83
Q

ARBs may have to be adjusted based on what?

A

the cytochrome P450 system of an individual

84
Q

What are indications for calcium channel blockers?

A
  • HTN
  • angina
  • rate control in FIB
  • supraventricular tachycardia (SVT)
  • raynaud syndrome
  • migraines (verapamil)
85
Q

What are the two types of calcium channel blockers?

A

dihydropyridine
non-dihydropyridine

86
Q

How do calcium channel blockers work?

A
  • decrease cardiac workload & myocardial O2 consumption
  • inhibits the movement of calcium across the membranes of the myocardial/ arterial muscle cells
  • alter action potential & block muscle cell contractions
  • decreases contractility & slow AV conduction
  • relax & dilate arteries
87
Q

dihydropyridine CCBs are more __________ ___________

A

vascular selective

88
Q

dihydropyridine CCBs have more of a direct effect on ____________ & less reduction of ____________

A

vasodilation; calcium

89
Q

dihydropyridine has no effect on __ __________ and may ________ HR due to vasodilation

A

AV contraction; decrease

90
Q

What do DIhyropyridine CCBs end in?

A

“Pine”

91
Q

Dihydropyridines CCBs don’t affect the _______ as much

92
Q

What are the side effects of dihydropyridine CCBs?

A

peripheral edema - common
headache
flushing
lightheadedness
dizziness
GI side effects
increased HR

93
Q

What should you not eat when taking CCBs?

A

grapefruit

94
Q

why should you not have grapefruit when taking CCBs?

A

increase the risk of hypotension

95
Q

What are the indications for non-dihydropyridine CCBs?

A
  • HTN
  • angina
  • arrhythmias ( a-Fib or SVT)
96
Q

Non-dihydropyridines CCBs have a _________ inotropic effect

97
Q

What are examples of dihydropyridine CCBs?

A

amlodipine
felodipine
nifedipine

98
Q

How do non-dihydropyridine CCBs work?

A
  • slow AV conduction & the rate of SA node
  • decrease force of contraction
99
Q

What are the two medications that are non-dihydropyridines CCBs?

A

verapamil
diltiazem

100
Q

How can both non-dihydropyridines be given?

A

both can be given IV

101
Q

What are the adverse effects of non-dihydropyridine CCBs?

A

bradycardia
decreased cardiac output
GI side effects

102
Q

When should non-dihydropyridine CCBs not be used?

A

should not be used in those with heart block

103
Q

What should be monitored when taking CCB?

104
Q

What can CCBs cause?

A

hypotension & bradcardia

105
Q

What are the nursing considerations for CCBs?

A
  • be aware of conduction issues
  • avoid grapefruit; especially with diltiazem
  • no lab monitoring
  • monitor for orthostatic hypotension
106
Q

What should you check before taking CCBs?

A

always do apical HR prior to administration; call MD if under 60

107
Q

When should you avoid using CCBs?

A

in those with HF

108
Q

What kind of medications does grapefruit inhibit?

A

CYP3A medications

109
Q

grapefruit can increase levels of med in the blood which increased risk of what?

A

iadverse effects & events

110
Q

When CYP3A meds are inhibited what happens?

A

there is decreased metabolism of the medication

111
Q

What kind of medications should not be taken with grapefruit?

A

oral antifungals
diltiazem
statins

112
Q

What are indications for beta blockers?

A
  • HTN (not first line)
  • decrease risk of sudden death after MI
  • all pt after MI & PCI
  • HR reduction in AFib
  • palpitations
  • HF
  • migraines
  • performance anxiety
  • hyperthyroidism
113
Q

What do beta blockers do?

A
  • decrease HR & BP
  • decrease muscle contraction
  • increase blood flow to the kidneys
  • decrease renin release
  • blocks SNS responses
114
Q

What do beta blockers end in?

A

“olol”

115
Q

What are adverse effects of beta blockers?

A

fatigue
depression
impotence
sleep issues
bradycardia

116
Q

What are the special uses of metoprolol?

A

HF & post MI

117
Q

What are the special uses of propranolol?

A

social anxiety & headaches

118
Q

Why should you check the glucose of someone on beta blockers?

A

beta blockers can mask hypoglycemia episodes

119
Q

With what respiratory condition should you use caution when taking beta blockers?

A

use in chronic lung disease; may increase risk of asthma attacks

120
Q

In what heart issue should you use caution with beta blockers?

A

in those with brady arrhythmias

121
Q

What should you do before administering beta blockers?

A

check apical pulse; call MD if under 60

122
Q

What should you never do when taking beta blockers?

A

never stop abruptly; pt should always be slowly weaned off to avoid sympathetic surge

123
Q

What are nursing considerations for beta blockers?

A
  • check for orthostatic hypotension
  • monitor glucose, esp if pt is diabetic
  • make sure pt is given med even when NPO
  • assess for side effects
  • no major lab concerns
124
Q

What are the medications that are selective beta 1 blockers?

A

metoprolol
atenolol
esmolol
bisoprolol

125
Q

What are the medications that are nonselective beta blockers (effects both 1 & 2 receptors)?

A

propanolol
carvedilol
nadolol
sotalol

126
Q

When are non- selective beta blockers contraindicated?

A
  • asthma
  • bronchospasms
  • heart failure
  • chronic lung disease
  • use in those with brady arrhythmias
127
Q

Cardio-selective beta blockers are ______ likely to have sx but ______ doses can cause lung sx

A

less; higher

128
Q

What are the two types of metoprolol?

A

succinate
tartrate

129
Q

What is metoprolol succinate used for?

A

tx of HF
tx of HTN

130
Q

is metoprolol succinate long or short acting?

A

long acting

131
Q

When is metoprolol succcinate usually usually taken?

A

usually dosed daily

132
Q

is metoprolol short or long acting?

A

short-acting

133
Q

When is metoprolol tartrate used?

A

used post MI
used for rate control in arrhythmias

134
Q

how can metoprolol tartrate be given?

135
Q

Can metoprolol succinate & tartrate be used interchangeably?

A

no; not unless order specifically

136
Q

What should you know when a pt is taking metoprolol?

A

if they are on succinate or tartrate

137
Q

What do alpha blockers do?

A
  • inhibit alpha synapse at the alpha adrenergic receptors (blocks SNS)
  • prevent feedback of norepinephrine
138
Q

What can alphia blockers do?

A

can block beta receptors

139
Q

Are alpha blockers used often of HTN?

A

not really used in BP control; considered 3rd-4th line tx

140
Q

What are alpha blockers really good at acting as?

A

work really well as antihypertensive

141
Q

What should you do when giving a pt an alpha blocker?

A

watch pt closely especially for the 1st hr; monitor for hypotension & bradycardia

142
Q

What are the adverse effects of alpha blockers?

A
  • first dose effect
  • syncope & dizziness
  • orthostatic hypotension
  • tachycardia
  • vertigo
  • sexual dysfunction
143
Q

What are the examples of alpha blockers?

A

doxazosin (cardura)
prazosin (minipress)

144
Q

In what population shoul you avoid giving alpha blockers and why?

A

avoid in use in older adults due to increased sedation/confusion