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Cardio exam 1 > HTN treatment lecture > Flashcards

HTN treatment lecture Flashcards

1
Q

essential (primary) HTN

A

unknown cause (90%)

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2
Q

secondary HTN

A 
identifiable cause (disease, drug, CKD, NSAIDs)
(5-10%)
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3
Q

white coat HTN

A

BP increases in a clinical setting, normal or low at home

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4
Q

pseudohypertension

A

BP falsely elevated due to rigid calcified brachial artery

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5
Q

osler’s maneuver

A

used to test for pseudohypertension.

BP cuff inflated above peak SBP, if radial artery remains palpable + osler’s (pseudohypertension)

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6
Q

isolated systolic HTN

A

only systolic is high

DBP is normal or low

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7
Q

resistant HTN

A

not at goal BP but on max dose of at least 3 drugs; one of which includes a diuretic

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8
Q

hypertensive crisis

A

> 180/120
Emergency if TOD- goal DBP<110 over min-hours with IV agents
urgency if no TOD- can use PO agents to decrease BP to stage 1 values over several hours

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9
Q

diagnosis of HTN is based on

A

2 reading taken on separate occasions

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10
Q

home readings over 5-7 days greater than ____ are abnormal

A

> 130/85

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11
Q

ambulatory BP monitoring (ABPM)

A

checks BP every 15 minutes over 24 hours

  • should drop 10-20% during sleep
  • > 130/85 abnormal
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12
Q

normal BP

A

<120/80

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13
Q

prehypertension

A

SBP 120-139 ot DBP 80-89

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14
Q

Stage 1

A

SBP 140-159 or DBP 90-99

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15
Q

stage 2

A

SBP >160 or DBP>100

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16
Q

major cardiovascular risk factors

A

HTN, obesity, dyslipidemia, DM, smoking, inactivity, albuminuria (GFR55 men, >65 women), family history

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17
Q

identifiable causes of HTN

A

sleep apnea, drug induced, primary alosteronism, renovascular disease, cushing syndrome, steroids, pheochomacytoma, CKD, thyroid/parathyroid disease, coarctation of aorta

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18
Q

diagnostic work up steps

A
  1. assess risk factors & co-morbidities
  2. reveal identifiable causes
  3. assess presence of target organ damage
  4. history & physical exam
    5/ baseline lab tests
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19
Q

lifestyle modification

A
  • weight reduction (normal BMI 18.5-24.9)
  • Dash diet
  • Na restriction (< 2400mg; <1 drink in women
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20
Q

BP goal for most patients

A

<140/90

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21
Q

BP goal for >80 & 60-80 who are frail

A

<150/90

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22
Q

BP goal for anyone who has DM or CKD

A

<140/90

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23
Q

compelling indications

A
  • left ventricular dysfunction
  • post MI
  • coronary artery disease
  • DM
  • CKD
  • recurrent stroke prevention
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24
Q

stage 1 therapy w/ no compelling indicators

A

monotherapy using ACEI, ARB, CCB, or thiazide

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25
Q

stage 1 black patients w/ no compelling indicators should be started on

A

CCB or thiazide

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26
Q

stage 2 therapy w/ no compelling indicators

A

2 drug combo for most

thiazide or CCB + ACEI or ARB

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27
Q

primary anihypertensives

A

ACEI, ARBs, thiazides, CCBs

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28
Q

alternative antihypertensives

A

beta-blockers, direct renin inhibitors, alpha-blockers (peripheral), central alpha2-agonst, adrenergic inhibitors, vasodilators

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29
Q

ALLHAT conclusions

A
  1. no difference in primary outcome or all-cause mortality
  2. ACEI less effective in black patients to decrease BP & CV outcomes (as mono therapy)
  3. chlorthalidone was the drug of choice bc decreased secondary outcomes & at the same time was least expensive
  4. more than 1 agent was required to control BP in most patients
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30
Q

diuretics have synergistic effect w/ other agents. esp:

A

ACEI/ARBs & beta-blockers

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31
Q

diuretic early BP decrease due to

A

diuresis

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32
Q

diuretic chronic BP decrease due to

A

decreased PR

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33
Q

1st generation thiazides not effective in

A

significant renal impairment (SCr >2.5, CrCl <30)

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34
Q

thiazides may be considered 1st line, esp in

A

blacks & elderly

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35
Q

thiazide most common side effects

A

hypokalemia, hypo-Mg, hyperuricemia

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36
Q

thiazide clinical pearls

A
  1. diuretic decreases w/ time
  2. takes 2-3 weeks to see max benefit
  3. chlrthalidone is ~1.5X more potent than HCTZ & has longer T1/2
  4. increase dose leads to increased electrolyte problems. generally limit HCTZ dose to 25mg/day
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37
Q

thiazide diuretics

A

HCTZ & chlorthalidone

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38
Q

Thiazide-like diuretics

A

indapamide & metolazone

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39
Q

loop diuretics

A

furosemide, torsemide, bumetamide

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40
Q

loop diuretics may be considered in uncomplicated HTN in patients with

A

significant renal dysfunction not responsive to thiazides

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41
Q

loop diuretic clinical pearls

A

limited routine use
biggest role is resistant HTN in presence of renal dysfunction
significant diuresis & electrolyte problems

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42
Q

potassium-sparing diuretic clinical pearls

A

primarily used with thiazides to decrease hypokalemia

may cause hyperkalemia, esp. in combo w/ ACEI/ARB

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43
Q

aldosterone antagonists (K-sparing) drugs

A

eplerenone & spironolactone

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44
Q

k- sparing drugs (Na channel)

A

amiloride, trimterene

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45
Q

aldosterone antagonists contraindications

A
  1. spironolactone should be avoided in CrCl 1.8 (women), >2(men), & T2DM w. albuminuria
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46
Q

aldosterone antagonist clinical pearls

A

may cause significant hyperkalemia, esp. w/ ACEI/ARB or K supplements

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47
Q

monitoring therapy for diuretics

A
  1. Chem7 (esp. Na, K, BUN, SCr, Glu)

2, base line, then in 1-2 weeks, then Q6-12 months or after initiating other agents

48
Q

ACEI affect on SCr

A

modest elevation (up to 35% normal)

49
Q

why pick ACEI first?

A

DM, CKD, HF, stroke, MI

50
Q

ACEI ADE

A

dry cough, angioedema, hypotension, renal dysfunction, hyperkalemia

51
Q

ACEI contraindications

A

prego (category C)
bilateral renal artery stenosis
avoid concurrent NSAID use if possible

52
Q

ACEI clinical pearls

A
  1. decrease or stabilize albuminuria-protective in DM
  2. chronic renal insufficiency is NOT a CI- start low and go slow
  3. monitor renal function & K
  4. limit salt intake
53
Q

NSAID effects

A
  • decrease GFR

- block prostaglandins that vasodilate afferent arteriole-> block afferent (ACEI/ARBs block efferent)

54
Q

ARB clinical pearls

A
  1. no cough & decreased risk of angioedema
  2. similar outcomes & ADE as ACEI
  3. renal data available in DM & CKD
  4. typically more expensive than ACEI
  5. do not use in combo with another RAS inhibitor
55
Q

DHP CCBs

A
  • may cause reflex tachyradia
  • pedal edema most common SE
  • peripheral vasodilatory effects
56
Q

non-DHP CCBs

A
  • cardiac effects
  • useful for supraventricular tachyarrhythmias
  • good coronary vasodilators
  • most common ADE: bradycardia & heart block
57
Q

non-DHP drugs

A

verapamil & diltiazem

58
Q

heart block

A

can go from bradycardia to a disease in the electrical system of the heart.

59
Q

DHP drugs

A

-pine

nifedipine, nicardipine, amlodipine, isradapine, felodipine, nisoldipine

60
Q

CCB clinical pearls

A
  1. may use DHP + nonDHP together
  2. constipation, esp. verapamil
  3. bc of cardiac effects, caution in cobo w/ beta-blockers & nonDHP
  4. avoid short-acting DHP
  5. watch for interactions (CYP450), esp. with verapamil & diltiazem
61
Q

can consider beta-blockers first line in what compelling indications

A

MI, heart failure, angina

high renin-hypertensives, arrhythmias, migraines, tremors, anxiety, thyrotoxicosis

62
Q

beta-blockers are less effective in

A

black patients

63
Q

beta1 selective beta-blockers

A 
atenolol
betaxolol
bisoprolol
metoprolol tartrate
metoprolol succinate
nevibolol
64
Q

nonselective beta-blockers

A

nadolol
propranolol
timolol

65
Q

intrinsic sympathomimetic beta-blockers

A

acebutolol
carteolol
penbutolol
pindolol

66
Q

mixed alpha & beta blockers

A

carvedilol

labetolol

67
Q

ADE of nonselective beta blockers (Beta 1)

A

bradycardia, heart block, acute heart failure

68
Q

ADE for B2 blocking

A

bronchospasms in asthma/COPD

cold extremities or aggravation of intermittent claudication or Raynaud’s phenomenon

69
Q

beta-blocker clinical pearls

A
  1. all lower BP to a similar extent
  2. cardio-selectivity is dose dependent & varies from patient to patient
  3. use selective agents in those w/ COPD/asthma- BAM (bisopropol, atenolol, metoprolol)
  4. do not abruptly withdraw
  5. use with extreme caution if also on a nonDHP- big time risk for bradycardia & potential heart block
70
Q

direct renin inhibitor

A

aliskiren

71
Q

direct renin inhibitor ADE & CIs

A

same as ACEI & ARBs

72
Q

direct renin inhibitor clinical pearls

A
  1. equally effective as ACEI & ARBs
  2. do not`want to use them with another RAS inhibitor (ACEI/ARB)
  3. no hard outcomes data
73
Q

alpha1 blocker MOA

A

block alpha1 receptors on blood vessels which causes vasodilation in periphery

74
Q

alpha1 blockers are

A

alternative agents which should be used in combo

75
Q

alpha1 blocker ADE

A

orthostatic hypotension, dizziness, palpitations

76
Q

alpha1 blocker drugs

A

doxazosin
prazosin
terazosin

77
Q

alpha1 blocker clinical pearls

A
  1. useful in mean with benign prostate hyperplasia (BPH)
  2. take 1st dose at bedtime
  3. may cayse Na-H2O retention- most effective when given with a diuretic
78
Q

alpha2 agonist clinical effects

A

decr. sympathetic tone, incr. PS activity-> < in HR, CO, PR, renin & barareceptor reflexes

79
Q

alpha2 receptors are mostly found where?

A

in the brain

80
Q

alpha 2 agonist drugs

A

clonidine
guanfacine
guanebenz
methyldopa

81
Q

alpha2 agonist ADE

A
  1. sedation & dry mouth
  2. CNS effects- depression, dizziness, orthostatic hypotension, anticholinergic effects (clonidine)
  3. Na-H2O repention (methyldopa)
82
Q

alpha2 agonist clinical pearls

A
  1. generally avoid when possible esp, in elderly bc of central effects
  2. methyldopa should be given w/ diuretic except in prego
  3. do not abruptly withdraw
  4. methyldopa may cause hepatitis or hemolytic anemia
83
Q

reserpine ADE

A
  1. significant Na/H2O retention
  2. may incr. nasal stuffiness, gastric acid secretion, diarrhea, & bradycardia due to incr. PS activity
  3. associated w/ incr. depression
84
Q

reserpine clinical pearls

A
  1. use with a diuretic

2. very inexpensive

85
Q

direct arterial vasodilator drugs

A

hydralazine & minoixil

86
Q

direct arterial vasodilator MOA

A

cause direct arterial SM relaxation. may activate barorecptors & incr. sympathetic outflow (> HR, CO, renin, <hypotenisve effect)

87
Q

direct arterial vasodilator ADE

A
  1. Na-H2O retention
  2. reflex tachycardia
  3. drug-induced lupus-like syndrome (hyralazine)
    hirsutism (minoxidil)
88
Q

direct arterial vasodilator clinical pearls

A
  1. use w/ beta blocker & diuretic- due to compensatory mechanisms
    2, monotherapy can precipitate angina-reflex tachycardia
  2. reserved for dificult to control HTN
89
Q

about what % of patients achieve goal BP with monotherapy?

A

<50%

90
Q

synergistic combinations

A

block compensatory mechanisms

91
Q

synergistic combinations

A
  1. RAS inhibitor + diuretic

2. CCB + RAS inhibitor

92
Q

additive combinations

A
  1. beta-blockers + diuretic
  2. beta-blocker + DHP CCB
  3. nonDHP +DHP
93
Q

less effective combinations

A
  1. diuretics + DHP CCB

2. beta-blockers + RAS inhibitors

94
Q

diuretics & DHP CCBs both

A

decrease PR

95
Q

beta-blockers & RAS inhibitors both

A

inhibit renin releae

96
Q

HTN in elderly is often

A

ISH (lead pipe syndrome)

- systolic is high, but diastolic is normal

97
Q

avoid what drugs in the elderly?

A

central acting agents & alpha blockers

98
Q

preeclampsia

A

increased BP with proteinuria

99
Q

most common drugs used in preeclampsia

A

methyldopa or labetolol

- beta-blockers, CCB, diuretics probably ok- not a lot of data

100
Q

Contraindicated in prego

A

ACEI, ARBs, direct Renin inhibitors

101
Q

standard for monitoring HTN

A

clinic BP monitoring

102
Q

BP response should be evaluted

A

2-4 weeks after initiating or changing therapy

-thiazides take 2-3 weeks to see max benefit

103
Q

diuretic monitoring

A

BP, BUN/SCr, electrolytes (k, Mg, Na)

104
Q

aldosterone antagonist monitoring

A

BP, BUN/SCr, K

105
Q

Beta-blocker monitoring

A

BP, HR

106
Q

ACEI/ARB/Renin inhibitor monitoring

A

BP, BUN/SCr, K

107
Q

CCB monitoring

A

BP, HR

108
Q

Possible 2* causes of resistant HTN

A
  1. non-adherence
  2. lifestyle & non-pharmacological modalities
  3. other meds
  4. other diseases
109
Q

medication considerations in unknown causes

A
  1. use synergistic or additive combos
  2. consider changing to loop
  3. add spionolactone
  4. combined alpha-beta blockers
  5. centrally acting agents
110
Q

renal parenchymal disease

A

ACEI/ARB+ loop;BB; CCB

111
Q

renal artery disease

A

angioplasty with stenting in unilateral disease & selected pts

112
Q

aldosteronism

A

aldosterone antagonists; ACEI/ARB; surgery for adenoma

113
Q

pheochromocytoma

A

alpha-adrenergic inhibitor; BB; surgical removal

114
Q

cushing’s syndrom

A

surgery

115
Q

hyper/hypo-thyroidism

A

treat underlying condition

116
Q

sleep apnea

A

weight loss; CPAP; possibly aldosterone antagonist

117
Q

coarctation of aorta

A

surgey

Cardio exam 1 (12 decks)

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