HTN 3 - olenik Flashcards

1
Q

what is the MOA of ACEi?

A

inhibits conversion for angiotensin I to angiotensin II

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2
Q

what does ACEi stand for?

A

angiotensin converting enzyme inhibitors

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3
Q

what is the MOA of ARBs?

A

block effects of angiotensin II by binding to target receptors

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4
Q

what does ARBs stand for?

A

angiotensin II receptor blockers

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5
Q

what is the MOA of renin inhibitors?

A

inhibits the conversion of angiotensinogen to angiotensin I

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6
Q

how does ACEi and ARBs effect HTN?

A

vasodilation
reduced PVR
increased diuresis

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7
Q

what disease states benefit from ACEi treatment?

A

Dm with proteinuria
post-MI
CKD

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8
Q

when should ACEi/ARBs be administered?

A

PM to ensuring BP dipping overnight

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9
Q

how often should ACEi be administered?

A

2-3x per day for Captopril
1-2x for everything else

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10
Q

what drugs are ACEi?

A

benazepril
captopril
enalapril
fosinopril
lisinopril
moexipril
perindopril
quinapril
ramipril
trandolapril

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11
Q

what are the SE of ACEi?

A

angioedema
cough (20%)
high K
acute renal failure with severe bilateral renal artery stenosis

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12
Q

what are the CIs of ACEi?

A

history of angioedema on ACEi
concomitant use of aliskiren in patients with DM
pregnancy/breastfeeding

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13
Q

what is the indication of ARBs?

A

HTN (first line but backup for ACEi if intolerant)

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14
Q

why do ARBs not produce a couhg?

A

does not block bradykinin breakdown

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15
Q

what drugs are ARBs?

A

azilsartan
candesartan
irbesartan
losartan
olmesartan
telmisartan
valsartan

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16
Q

how often should ARBs be administered?

A

1-2 times for losartan
1 qd for everything else

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17
Q

what are SE of ARBs?

A

angioedema
high K
acute renal failure with severe bilateral renal artery stenosis

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18
Q

what are the CIs of ARBs?

A

history of angioedema on an ARB
concomitant use of aliskiren in patients with DM
pregnancy/breastfeeding

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19
Q

how should ACEi/ARBs be monitored?

A

potassium and renal function
at baseline
at 1-2 weeks after initiation if elderly
at 3-4 weeks after initiation for low-risk patients, patients with potassium under 4.5, or if elevated SCr in elderly at 1-2 weeks
every 6-12 months

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20
Q

when should ACEi/ARBs be held or reduced in dose?

A

when K is greater than 5.5
SCr increases by 30%

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21
Q

what is indication of direct renin inhibitors?

A

not first-line for HTN due to cost and simialr efficacy
less cough than ACEi

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22
Q

what drug is a direct renin inhibitor?

A

Aliskiren

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23
Q

how should aliskiren be dosed?

A

qd

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24
Q

what are the CI of aliskiren?

A

pregnancy
concomitant use with ACEi or ARB in patients with DM

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25
Q

what should be monitored when taking aliskiren?

A

K
BUN
SCr

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26
Q

what are SE of aliskiren?

A

diarrhea
musculoskeletal effects (CK increase)
dizziness
HA
high K
renal insufficiency/ARF
orthostatic hypotension

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27
Q

what are the clinical pearls of angiotensin inhibitors?

A

discuss contraceptive methods with women at childbearing age
do not combine drug classes due to risk of SE
assess patients risk for hyperkalemia (CKD, other meds)
educate patient on dietary source of potassium (bananas, food seasoning)
ACEi/ARBs often preferred over other first line agents in the presence of other compelling indications

28
Q

what is the MOA of CCBs?

A

inhibit influx of calcium across cardiac and smooth muscle cell membranes
leads to coronary and peripheral vasodilation

29
Q

what does CCB stand for?

A

calcium channel blockers

30
Q

what are subclasses of CCBs?

A

dihydropyridines (more vasodilation)
nondihydrophyridines (more negative ionotropic effects)

31
Q

what is the indication of CCBs?

A

first line for HTN

32
Q

what populations would benefit the most from using dihydropyridine CCBs?

A

reynaud’s syndrome
elderly pts with isolated systolic HTN

33
Q

how are dihydropyridine CCBs dosed?

A

BID for isradipine and nicardipine
QD for everything else

34
Q

what drugs are dihydropyridine CCBs?

A

amlodipine
felodipine
isradipine
isradipine SR
nicardipine SR
nifedipine LA
nisoldipine

35
Q

what dihydropyridine CCBs have no negative ionotropic effects?

A

amlodipine
felodipine

36
Q

how does dihydropyridine CCBs effect HTN?

A

vasodilation
baroreceptor mediated tachycardia
no effect on atrioventricular node conduction

37
Q

what dihydropyridines should be avoided in HTN?

A

short-acting ones like IR nifedipine/nicardipine

38
Q

what are the SE of dihydropyridine CCBs?

A

reflex tachycardia
flushing
dizziness
HA
peripheral edema (dose-related)
gingival hyperplasia

39
Q

what are the warnings of dihydropyridine CCBs?

A

increased risk of angina/MI in patients with obstructive coronary disease due to reflex tachycardia

40
Q

what are the drug-drug interactions of dihydropyridine CCBs?

A

grapefruit juice
CYP3A4 enzyme inducers/inhibitors

41
Q

what populations may benefit from nondihydropyridine CCBs?

A

supraventricular tachyarrhythmias (Afib)
patients with angina who cannot tolerate a beta blocker

42
Q

what are the effects of nondihydropyridine CCBs?

A

slows AV node conduction
decreases heart rate –> negative ionotropic effects

43
Q

what type of tablet is preferred in nondihydropyridine CCBs?

A

extended release

44
Q

what drugs are nondihydropyridine CCBs?

A

diltiazem ER
verapamil ER

45
Q

how should nondihydropyridines be dosed?

A

QD to BID

46
Q

what are the SE of nondihydropyridines CCBs be dosed?

A

bradycardia
HA
dizziness
AV node block
systolic HF
gingival hyperplasia
constipation (verapamil > diltiazem)

47
Q

what are the drug-drug interactions of nondihydropyridine CCBs?

A

concomitant use of beta blockers (could increase risk of heart block)
grapefruit juice
CYP3A4 enzyme inducers/inhibitors

48
Q

what are the CI of nondihydropyridine CCBs?

A

heart block
left ventricular dysfunction

49
Q

what are the clinical pearls of CCBs?

A

no routine laboratory monitoring required
check for drug interactions
CCBs are first line for HTN
peripheral edema is dose-dependent
ER formulations are preferred
nondihydropyridine CCB formulations are not interchangeable
if a CCB is needed in the HF choose amlodipine

50
Q

when should beta blockers be used in HTN?

A

not first line unless a compelling indication is present such as HF and CAD

51
Q

what populations would benefit from beta blockers?

A

tachyarrhythmias
tremors
migraines
thyrotoxicosis

52
Q

how does beta blockers effect HTN?

A

decreases HR, force of contraction, and CO

53
Q

what are the clinical pearls of beta blockers?

A

avoid abrupt cessation

54
Q

what drugs are cardioselective beta blockers?

A

atenolol
betaxolol
bisoprolol
metoprolol tartrate
metoprolol succinate
nebivolol

55
Q

how is nebivolol unqiue?

A

has nitric oxide-induced vasodilation

56
Q

how should cardioselective beta blockers be dosed?

A

BID for metoprolol tartrate
QD for everything else

57
Q

what drugs are nonselective beta blockers?

A

nadolol
propranolol IR
propranolol LA

58
Q

what are the CI of nonselective beta blockers?

A

bronchospastic airway disease

59
Q

how should nonselective beta blockers be dosed?

A

BID propranolol IR
QD everything else

60
Q

what drugs are beta blockers with intrinsic sympathomimetic activity (ISA)?

A

acebutolol
penbutolol
pindolol

61
Q

what are the CI of beta blockers with ISA?

A

heart failure
IHD

62
Q

how should beta blockers with ISA be dosed?

A

BID acebutolol, pindolol
QD penbutolol

63
Q

what drugs are beta blockers with mixed alpha/beta activity?

A

carvedilol
labetalol

64
Q

how should mixed alpha/beta activity beta blockers be dosed?

A

BID

65
Q

what are SE of beta blockers?

A

bronchospasms
bradycardia
fatigue
exercise intolerance
depression
can masked signs and symptoms of hypoglycemia

66
Q

what populations should use caution of beta blockers?

A

peripheral artery disease (carvedilol preferred)
reactive airway disease (use selective beta blockers)

67
Q

what are the CI of beta blockers?

A

second or third degree heart block
decompensated heart failure
post MI (ISA BBs only)
severe bradycardia
sick sinus syndrome