Hypertension Flashcards

(109 cards)

1
Q

new HTN goal

A

<130/80

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2
Q

initial monotherapy for black population

A

Thiazide diuretic or CCB

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3
Q

initial monotherapy for non-black population

A

thiazide diuretic, ACEI, ARB, CCB

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4
Q

initial monotherapy for black or non-blacks with CKD

A

ACEI, ARB

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5
Q

validated BP monitors with memory

A

lifesource, Omron

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6
Q

when should pts take their blood pressure

and how many times

A

before taking BP meds, 30+ min after exercise, smoking, caffeine
2-3 readings 1 min apart

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7
Q

what do blacks respond less to

A

ACEI, ARB, B blocker

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8
Q

preferred combos

A

ACEI, ARB + thiazide

ACEI, ARB + DHP- CCB

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9
Q

generally, combos that are not preferred

A

do not combine anything else with ACEI or ARB besides thiazide or DHP-CCB
do not combine b-blockers with ACEI, ARB, non-DHP CCB, or central acting agonists (clonidine)

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10
Q

meds that induce HTN

A
OCPs
stimulants 
transplant meds (cyclosporine) 
EPO
corticosteroids
NSAIDS
sympathomimetics (decongestants) 
neuropsych meds
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11
Q

how to evaluate med adherence

A
1 identify ADRS, switch therapy
2 evaluate cost 
3 explain importance of BP management 
4 get pts engaged 
5 pharmacy automatic refil program
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12
Q

what is chronotherapy and why do we use it

A

taking 1 or more BP med at night - ok to do if they are on >1 BP med
may prevent morning BP rise or help pts whos BP doesn’t dip at night like it should

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13
Q

diuresis vs natriuresis

A

diuresis: increase urine volume
natriuresis: increase renal Na excretion

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14
Q

Mannitol indications

A

decrease ICP from cerebral edema

GU irrigate in TURP or transurethral surg procedure

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15
Q

acetazolamide indications

A

acute mountain sickness

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16
Q

loop diuretics

A

furosemide (Lasix)
torsemide
bumetanide
ethacrynic acid

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17
Q

loop diuretic MOA

A

inhibits Na/K-ATPase pump in thick segment of loop of henle

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18
Q

indications for loop diuretics

A
  • acute pulmonary edema
  • edema states
  • acute hypercalcemia
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19
Q

monitoring for loop diuretics

A
  • BMP
  • Ca, Mg
  • daily weights
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20
Q

effectiveness of loops vs thiazides in HF + why

A

loops > thiazides for HF b/c more Na+ excretion

loops > thiazides for GFR < 30 mL/min

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21
Q

starting dose for loops

A

20-40 mg up to 80 mg q AM
“double the dose until the urine flows”
then consider a second dose in afternoon

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22
Q

what to add onto loop diuretic if eGFR < 30

A

metolazone (thiazide)

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23
Q

what to add onto loop diuretic if eGFR >30

A

spironolactone

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24
Q

ADR of ethacrynic acid

A

ototoxicity

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25
benefits of ethacrynic acid
for pts who have not responded to other diuretics | only loop without a "sulfa group"
26
interactions for loop diuretics
* NSAIDS antagonize diuretic effect via Na retention * loops antagonize DM meds via hypokalemia - anti-arrhythmic and lithium toxicity - antagonizes gout meds - anti-htn, vasodilators
27
loop ADRs
- hypokalemia, hypomagnesemia, hypo k metabolic alkalosis - hyperglycemia - volume depletion - hyponatremia - hyperuricemia - SNHL (ethacrynic acid >) - rash
28
thiazide diuretics
hydrochlorothiazide chlorthalidone metolazone (indapamide, chlorothiazide)
29
thiazide MOA
inhibits NA/K-ATPase pump in distal convoluted tubule
30
chlorthalidone vs HCTZ
chlorthalidone 2x as potent as HCTZ, longer duration of action
31
why is HCTZ still more common
because it is the thiazide most often used in combo drugs
32
thiazide indications
HTN (dose in AM)
33
thiazide monitoring
- BMP - Ca, Mg - daily weights
34
effectiveness of diuretics when eGFR < 30
loops > thiazides *except metolazone*
35
what do thiazides do to calcium
enhance calcium reabsorption may unmask underlying condition improvement in hypercalciuria --> decrease in kidney stones
36
metolazone use
added to loop diuretics for synergy in refractory edematous states
37
thiazide ADRs
- hypokalemia, hypomagnesemia - volume depletion - hyperglycemia - hyperuricemia - hyperlipidemia - rash
38
anti-aldosterone potassium- sparing diuretics
spironolactone | eplerenone
39
potassium-sparing diuretics
amiloride | triamterene
40
anti-aldosterone K-sparing diuretic MOA
blocks aldosterone effects by antagonizing mineralocorticoid receptors at cortical collecting tubule
41
amiloride, triamterene MOA
inhibits Na/K-ATPase pump in cortical collecting tubule & collecting duct
42
amiloride, triamterene use
prevent/correct hypokalemia with other diuretics | has a week diuretic/BP effect
43
spironolactone, eplerenone use
1 primary aldosteronism 2 secondary aldosteronism 3 acne, hirsutism (off-label)
44
contraindications for K-sparing diuretic
K+ > 5.5 or eGFR <30
45
monitoring for K-sparing diuretic
K+, BUN/Cr
46
other drugs that retain K+
B-blockers Bactrim (TMP/SMX) NSAIDs, ACEI, ARBS
47
spironolactone ADRs
teratogenic estrogenic effects (gynecomastia, amenorrhea) anti-androgen effects
48
triamterene ADR
nephrotoxic --> crystalluria, cast formation
49
what are the two diuretics typically used together
loops + metolazone = synergistic
50
QD ACEi
lisinopril
51
what ACEi is a prodrug
enalapril
52
list of ACEi
``` lisinopril enalapril captopril benazepril fosinopril ...anything with PRIL ```
53
MOA of ACEi
- inhibits conversion of angiotensin I to angiotensin II by inhibiting ACE (from lung) = no increase in sympathetic activity, decreases water/Na reabsorption, inhibits vasoconstriction and increase in BP also vasodilates efferent arteriole and decreases glomerular pressure
54
ACEi indications
HTN (LVH>) HF with systolic dysfunction CKD post-AMI (with resulted decrease in systolic fcn)
55
ACEi + ARB are not only BP meds, they are also...
renal "protectors"
56
ACEi are synergistic with...
diuretics
57
ACEi/ARB monitoring
BMP/Cr, K+
58
contraindications for ACEi
bilateral RAS, stenotic lesion | pts with hereditary/idiopathic angioedema
59
ACEi ADRs
cough, angioedema teratogenic renal function decline hyperkalemia
60
ACEi cough characteristics (when, how long, epidemiology)
1-2 weeks into treatment as long as 6 months women > men
61
what is an acceptable increase of SCr when starting an ACEi
up to 30% increase from baseline is acceptable
62
angioedema is more common in...
black pts
63
when is an ARB in place of ACEi acceptable if the pt gets ACEi angioedema
if the angioedema symptoms were mild (swelling of face or tongue)
64
how long should you wait to switch from ACE to ARB from ACEi angioedema
>4 weeks to make sure angioedema has stopped
65
ARBs list
losartan - best data valsartan candesartan (other -SARTANS)
66
ARB MOA
impairs binding of angiotensin II to AT1 receptors = blocked vasoconstricting and aldosterone-secreting effects
67
what is an added indication for losartan
uricosuric activity - gout prevention
68
risk of cough/angioedema in ARB
less than ACEi
69
renin inhibitor
aliskiren
70
aliskiren MOA
binds to catalytic site of renin --> inhibits formation of angiotensin I/II and decreases plasma renin activity
71
monitoring for aliskiren
BUN/Cr, K+
72
should you combine an ACE + ARB or Aliskiren with ACE/ARB
nah
73
a-adrenergic antagonists (& long or short acting)
long-acting: terazosin, doxazosin | short acting: prazosin
74
what is common with a-blockers if they are not combined with a diuretic
fluid retention
75
a-blocker MOA
a1-receptor antagonist = decreased arterial PSI by dilating resistance and capacitance vessels
76
a-blockers indications
BPH (but now Tamsulosin >>) "medical expulsive therapy" for ureteral stones HTN (less use, poor data) prazosin - PTSD in combat veterans?
77
ADRs for a-blockers (when used for BPH)
``` *postural hypotension/dizziness (1st few doses >>) drowsiness/fatigue *nasal congestion/rhinitis retrograde ejaculation floppy iris syndrome ```
78
non-selective B-blockers
propranolol timolol nadolol
79
cautions when using nonselective B-blockers
COPD, asthma, raynauds pts
80
selective B1-blockers
metoprolol
81
tartrate vs succinate
tartrate - IR - dosed BID-TID | succinate - ER - dosed QD (used for HF)
82
nonselective B-blockers with a1-blocking activity
carvedilol | labetalol
83
selective b-blockers with increase NO release from endothelial cells
nebivolol
84
b-blockers MOA
competitive inhibitors of catecholamines at B-receptors
85
B1 receptors vs B2 receptors
B1- heart = increase HR/contractility/AV conduction | B2 - bronchial, peripheral vascular smooth muscle > heart muscle = vasodilation, bronchodilation
86
indications for B-blockers
HTN + angina HTN + a-fib HTN + HFrEF
87
additional uses for B-blockers
propranolol - infantile hemangiomas migraines essential tremor pheo/hyperthyroidism
88
when stopping B-blockers
taper over 1-2 weeks | can cause angina, AMI
89
who else are B-blockers contraindicated in
pts with 2nd/3rd degree heart block, SSS, bradycardia <50 bpm
90
important interaction of B-blocker
blunts effects of epi (EpiPen)
91
b-blocker ADRs
``` hyperkalemia bradycardia fatigue/exercise intolerance floppy iris syndrome bronchospasm ```
92
b-blockers may mask/delay recovery from...
hypoglycemia (non-selective) | *careful in diabetics
93
non-dhp ccbs
verapamil | diltiazem
94
dhp ccbs (and short v long acting)
short acting: nifedipine | long acting: amlodipine
95
CCB MOA
relax arterial smooth muscle, produce peripheral vasodilation via inhibiting L-type calcium channel
96
where do DHP CCBs act primarily
in vascular smooth muscle to decrease PVR
97
where do NON-DHP CCBs act primarily
effects cardiac contractility (verapamil>diltiazem) | less potent vasodilator
98
indications for DHP CCBs
HTN angina raynauds
99
indications for NON-DHP CCBs
cardiac arrhythmias | cluster HA prophylaxis - verapamil
100
who should you not use NON-DHP CCBs in
2nd/3rd degree heart block SSS bradycardia <50 HF
101
CCB class effect ADRs
peripheral edema, reflex tachycardia, HA, dizziness, flushing
102
verapamil ADR
constipation
103
nifedipine ADR
gingival hyperplasia
104
central a-adrenergic agonists
clonidine | methyldopa
105
a-agonist ADRs
dry mouth, sedation | HTN crisis if abrupt withdrawl
106
direct vasodilators
hydralazine | minoxidil
107
direct vasodilator MOA
relaxes arterial smooth muscle--> decreases PVR
108
hydralazine indications
- HTN - pre-eclampsia/eclampsia - HF (hydralazine + isosorbide dinitrate = BiDil)
109
what should you combine direct vasodilators with and why
B-blocker or centrally-acting drug - minimizes reflex increase in HR/CO diuretic - avoid Na, H20 retention