Hypertension Flashcards
new HTN goal
<130/80
initial monotherapy for black population
Thiazide diuretic or CCB
initial monotherapy for non-black population
thiazide diuretic, ACEI, ARB, CCB
initial monotherapy for black or non-blacks with CKD
ACEI, ARB
validated BP monitors with memory
lifesource, Omron
when should pts take their blood pressure
and how many times
before taking BP meds, 30+ min after exercise, smoking, caffeine
2-3 readings 1 min apart
what do blacks respond less to
ACEI, ARB, B blocker
preferred combos
ACEI, ARB + thiazide
ACEI, ARB + DHP- CCB
generally, combos that are not preferred
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)
meds that induce HTN
OCPs stimulants transplant meds (cyclosporine) EPO corticosteroids NSAIDS sympathomimetics (decongestants) neuropsych meds
how to evaluate med adherence
1 identify ADRS, switch therapy 2 evaluate cost 3 explain importance of BP management 4 get pts engaged 5 pharmacy automatic refil program
what is chronotherapy and why do we use it
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
diuresis vs natriuresis
diuresis: increase urine volume
natriuresis: increase renal Na excretion
Mannitol indications
decrease ICP from cerebral edema
GU irrigate in TURP or transurethral surg procedure
acetazolamide indications
acute mountain sickness
loop diuretics
furosemide (Lasix)
torsemide
bumetanide
ethacrynic acid
loop diuretic MOA
inhibits Na/K-ATPase pump in thick segment of loop of henle
indications for loop diuretics
- acute pulmonary edema
- edema states
- acute hypercalcemia
monitoring for loop diuretics
- BMP
- Ca, Mg
- daily weights
effectiveness of loops vs thiazides in HF + why
loops > thiazides for HF b/c more Na+ excretion
loops > thiazides for GFR < 30 mL/min
starting dose for loops
20-40 mg up to 80 mg q AM
“double the dose until the urine flows”
then consider a second dose in afternoon
what to add onto loop diuretic if eGFR < 30
metolazone (thiazide)
what to add onto loop diuretic if eGFR >30
spironolactone
ADR of ethacrynic acid
ototoxicity
benefits of ethacrynic acid
for pts who have not responded to other diuretics
only loop without a “sulfa group”
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
loop ADRs
- hypokalemia, hypomagnesemia, hypo k metabolic alkalosis
- hyperglycemia
- volume depletion
- hyponatremia
- hyperuricemia
- SNHL (ethacrynic acid >)
- rash
thiazide diuretics
hydrochlorothiazide
chlorthalidone
metolazone
(indapamide, chlorothiazide)
thiazide MOA
inhibits NA/K-ATPase pump in distal convoluted tubule
chlorthalidone vs HCTZ
chlorthalidone 2x as potent as HCTZ, longer duration of action
why is HCTZ still more common
because it is the thiazide most often used in combo drugs
thiazide indications
HTN (dose in AM)
thiazide monitoring
- BMP
- Ca, Mg
- daily weights
effectiveness of diuretics when eGFR < 30
loops > thiazides except metolazone
what do thiazides do to calcium
enhance calcium reabsorption
may unmask underlying condition
improvement in hypercalciuria –> decrease in kidney stones
metolazone use
added to loop diuretics for synergy in refractory edematous states
thiazide ADRs
- hypokalemia, hypomagnesemia
- volume depletion
- hyperglycemia
- hyperuricemia
- hyperlipidemia
- rash
anti-aldosterone potassium- sparing diuretics
spironolactone
eplerenone
potassium-sparing diuretics
amiloride
triamterene
anti-aldosterone K-sparing diuretic MOA
blocks aldosterone effects by antagonizing mineralocorticoid receptors at cortical collecting tubule
amiloride, triamterene MOA
inhibits Na/K-ATPase pump in cortical collecting tubule & collecting duct
amiloride, triamterene use
prevent/correct hypokalemia with other diuretics
has a week diuretic/BP effect
spironolactone, eplerenone use
1 primary aldosteronism
2 secondary aldosteronism
3 acne, hirsutism (off-label)
contraindications for K-sparing diuretic
K+ > 5.5 or eGFR <30
monitoring for K-sparing diuretic
K+, BUN/Cr
other drugs that retain K+
B-blockers
Bactrim (TMP/SMX)
NSAIDs, ACEI, ARBS
spironolactone ADRs
teratogenic
estrogenic effects (gynecomastia, amenorrhea)
anti-androgen effects
triamterene ADR
nephrotoxic –> crystalluria, cast formation
what are the two diuretics typically used together
loops + metolazone = synergistic
QD ACEi
lisinopril
what ACEi is a prodrug
enalapril
list of ACEi
lisinopril enalapril captopril benazepril fosinopril ...anything with PRIL
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
ACEi indications
HTN (LVH>)
HF with systolic dysfunction
CKD
post-AMI (with resulted decrease in systolic fcn)
ACEi + ARB are not only BP meds, they are also…
renal “protectors”
ACEi are synergistic with…
diuretics
ACEi/ARB monitoring
BMP/Cr, K+
contraindications for ACEi
bilateral RAS, stenotic lesion
pts with hereditary/idiopathic angioedema
ACEi ADRs
cough, angioedema
teratogenic
renal function decline
hyperkalemia
ACEi cough characteristics (when, how long, epidemiology)
1-2 weeks into treatment
as long as 6 months
women > men
what is an acceptable increase of SCr when starting an ACEi
up to 30% increase from baseline is acceptable
angioedema is more common in…
black pts
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)
how long should you wait to switch from ACE to ARB from ACEi angioedema
> 4 weeks to make sure angioedema has stopped
ARBs list
losartan - best data
valsartan
candesartan
(other -SARTANS)
ARB MOA
impairs binding of angiotensin II to AT1 receptors = blocked vasoconstricting and aldosterone-secreting effects
what is an added indication for losartan
uricosuric activity - gout prevention
risk of cough/angioedema in ARB
less than ACEi
renin inhibitor
aliskiren
aliskiren MOA
binds to catalytic site of renin –> inhibits formation of angiotensin I/II and decreases plasma renin activity
monitoring for aliskiren
BUN/Cr, K+
should you combine an ACE + ARB or Aliskiren with ACE/ARB
nah
a-adrenergic antagonists (& long or short acting)
long-acting: terazosin, doxazosin
short acting: prazosin
what is common with a-blockers if they are not combined with a diuretic
fluid retention
a-blocker MOA
a1-receptor antagonist = decreased arterial PSI by dilating resistance and capacitance vessels
a-blockers indications
BPH (but now Tamsulosin»_space;)
“medical expulsive therapy” for ureteral stones
HTN (less use, poor data)
prazosin - PTSD in combat veterans?
ADRs for a-blockers (when used for BPH)
*postural hypotension/dizziness (1st few doses >>) drowsiness/fatigue *nasal congestion/rhinitis retrograde ejaculation floppy iris syndrome
non-selective B-blockers
propranolol
timolol
nadolol
cautions when using nonselective B-blockers
COPD, asthma, raynauds pts
selective B1-blockers
metoprolol
tartrate vs succinate
tartrate - IR - dosed BID-TID
succinate - ER - dosed QD (used for HF)
nonselective B-blockers with a1-blocking activity
carvedilol
labetalol
selective b-blockers with increase NO release from endothelial cells
nebivolol
b-blockers MOA
competitive inhibitors of catecholamines at B-receptors
B1 receptors vs B2 receptors
B1- heart = increase HR/contractility/AV conduction
B2 - bronchial, peripheral vascular smooth muscle > heart muscle = vasodilation, bronchodilation
indications for B-blockers
HTN + angina
HTN + a-fib
HTN + HFrEF
additional uses for B-blockers
propranolol - infantile hemangiomas
migraines
essential tremor
pheo/hyperthyroidism
when stopping B-blockers
taper over 1-2 weeks
can cause angina, AMI
who else are B-blockers contraindicated in
pts with 2nd/3rd degree heart block, SSS, bradycardia <50 bpm
important interaction of B-blocker
blunts effects of epi (EpiPen)
b-blocker ADRs
hyperkalemia bradycardia fatigue/exercise intolerance floppy iris syndrome bronchospasm
b-blockers may mask/delay recovery from…
hypoglycemia (non-selective)
*careful in diabetics
non-dhp ccbs
verapamil
diltiazem
dhp ccbs (and short v long acting)
short acting: nifedipine
long acting: amlodipine
CCB MOA
relax arterial smooth muscle, produce peripheral vasodilation via inhibiting L-type calcium channel
where do DHP CCBs act primarily
in vascular smooth muscle to decrease PVR
where do NON-DHP CCBs act primarily
effects cardiac contractility (verapamil>diltiazem)
less potent vasodilator
indications for DHP CCBs
HTN
angina
raynauds
indications for NON-DHP CCBs
cardiac arrhythmias
cluster HA prophylaxis - verapamil
who should you not use NON-DHP CCBs in
2nd/3rd degree heart block
SSS
bradycardia <50
HF
CCB class effect ADRs
peripheral edema, reflex tachycardia, HA, dizziness, flushing
verapamil ADR
constipation
nifedipine ADR
gingival hyperplasia
central a-adrenergic agonists
clonidine
methyldopa
a-agonist ADRs
dry mouth, sedation
HTN crisis if abrupt withdrawl
direct vasodilators
hydralazine
minoxidil
direct vasodilator MOA
relaxes arterial smooth muscle–> decreases PVR
hydralazine indications
- HTN
- pre-eclampsia/eclampsia
- HF (hydralazine + isosorbide dinitrate = BiDil)
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
