Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology PaxFlan > Hypertension > Flashcards

Hypertension Flashcards

1
Q

new HTN goal

A

<130/80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

initial monotherapy for black population

A

Thiazide diuretic or CCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

initial monotherapy for non-black population

A

thiazide diuretic, ACEI, ARB, CCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

initial monotherapy for black or non-blacks with CKD

A

ACEI, ARB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

validated BP monitors with memory

A

lifesource, Omron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what do blacks respond less to

A

ACEI, ARB, B blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

preferred combos

A

ACEI, ARB + thiazide

ACEI, ARB + DHP- CCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

meds that induce HTN

A 
OCPs
stimulants 
transplant meds (cyclosporine) 
EPO
corticosteroids
NSAIDS
sympathomimetics (decongestants) 
neuropsych meds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

diuresis vs natriuresis

A

diuresis: increase urine volume
natriuresis: increase renal Na excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mannitol indications

A

decrease ICP from cerebral edema

GU irrigate in TURP or transurethral surg procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acetazolamide indications

A

acute mountain sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

loop diuretics

A

furosemide (Lasix)
torsemide
bumetanide
ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

loop diuretic MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

indications for loop diuretics

A
  • acute pulmonary edema
  • edema states
  • acute hypercalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

monitoring for loop diuretics

A
  • BMP
  • Ca, Mg
  • daily weights
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what to add onto loop diuretic if eGFR < 30

A

metolazone (thiazide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what to add onto loop diuretic if eGFR >30

A

spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ADR of ethacrynic acid

A

ototoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

benefits of ethacrynic acid

A

for pts who have not responded to other diuretics

only loop without a “sulfa group”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

interactions for loop diuretics

A
  • NSAIDS antagonize diuretic effect via Na retention
  • loops antagonize DM meds via hypokalemia
  • anti-arrhythmic and lithium toxicity
  • antagonizes gout meds
  • anti-htn, vasodilators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

loop ADRs

A
  • hypokalemia, hypomagnesemia, hypo k metabolic alkalosis
  • hyperglycemia
  • volume depletion
  • hyponatremia
  • hyperuricemia
  • SNHL (ethacrynic acid >)
  • rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

thiazide diuretics

A

hydrochlorothiazide
chlorthalidone
metolazone
(indapamide, chlorothiazide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

thiazide MOA

A

inhibits NA/K-ATPase pump in distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

chlorthalidone vs HCTZ

A

chlorthalidone 2x as potent as HCTZ, longer duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

why is HCTZ still more common

A

because it is the thiazide most often used in combo drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

thiazide indications

A

HTN (dose in AM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

thiazide monitoring

A
  • BMP
  • Ca, Mg
  • daily weights
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

effectiveness of diuretics when eGFR < 30

A

loops > thiazides except metolazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what do thiazides do to calcium

A

enhance calcium reabsorption
may unmask underlying condition
improvement in hypercalciuria –> decrease in kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

metolazone use

A

added to loop diuretics for synergy in refractory edematous states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

thiazide ADRs

A
  • hypokalemia, hypomagnesemia
  • volume depletion
  • hyperglycemia
  • hyperuricemia
  • hyperlipidemia
  • rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

anti-aldosterone potassium- sparing diuretics

A

spironolactone

eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

potassium-sparing diuretics

A

amiloride

triamterene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

anti-aldosterone K-sparing diuretic MOA

A

blocks aldosterone effects by antagonizing mineralocorticoid receptors at cortical collecting tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

amiloride, triamterene MOA

A

inhibits Na/K-ATPase pump in cortical collecting tubule & collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

amiloride, triamterene use

A

prevent/correct hypokalemia with other diuretics

has a week diuretic/BP effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

spironolactone, eplerenone use

A

1 primary aldosteronism
2 secondary aldosteronism
3 acne, hirsutism (off-label)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

contraindications for K-sparing diuretic

A

K+ > 5.5 or eGFR <30

45
Q

monitoring for K-sparing diuretic

A

K+, BUN/Cr

46
Q

other drugs that retain K+

A

B-blockers
Bactrim (TMP/SMX)
NSAIDs, ACEI, ARBS

47
Q

spironolactone ADRs

A

teratogenic
estrogenic effects (gynecomastia, amenorrhea)
anti-androgen effects

48
Q

triamterene ADR

A

nephrotoxic –> crystalluria, cast formation

49
Q

what are the two diuretics typically used together

A

loops + metolazone = synergistic

50
Q

QD ACEi

A

lisinopril

51
Q

what ACEi is a prodrug

A

enalapril

52
Q

list of ACEi

A 
lisinopril
enalapril 
captopril 
benazepril 
fosinopril
...anything with PRIL
53
Q

MOA of ACEi

A
  • 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
Q

ACEi indications

A

HTN (LVH>)
HF with systolic dysfunction
CKD
post-AMI (with resulted decrease in systolic fcn)

55
Q

ACEi + ARB are not only BP meds, they are also…

A

renal “protectors”

56
Q

ACEi are synergistic with…

A

diuretics

57
Q

ACEi/ARB monitoring

A

BMP/Cr, K+

58
Q

contraindications for ACEi

A

bilateral RAS, stenotic lesion

pts with hereditary/idiopathic angioedema

59
Q

ACEi ADRs

A

cough, angioedema
teratogenic
renal function decline
hyperkalemia

60
Q

ACEi cough characteristics (when, how long, epidemiology)

A

1-2 weeks into treatment
as long as 6 months
women > men

61
Q

what is an acceptable increase of SCr when starting an ACEi

A

up to 30% increase from baseline is acceptable

62
Q

angioedema is more common in…

A

black pts

63
Q

when is an ARB in place of ACEi acceptable if the pt gets ACEi angioedema

A

if the angioedema symptoms were mild (swelling of face or tongue)

64
Q

how long should you wait to switch from ACE to ARB from ACEi angioedema

A

> 4 weeks to make sure angioedema has stopped

65
Q

ARBs list

A

losartan - best data
valsartan
candesartan
(other -SARTANS)

66
Q

ARB MOA

A

impairs binding of angiotensin II to AT1 receptors = blocked vasoconstricting and aldosterone-secreting effects

67
Q

what is an added indication for losartan

A

uricosuric activity - gout prevention

68
Q

risk of cough/angioedema in ARB

A

less than ACEi

69
Q

renin inhibitor

A

aliskiren

70
Q

aliskiren MOA

A

binds to catalytic site of renin –> inhibits formation of angiotensin I/II and decreases plasma renin activity

71
Q

monitoring for aliskiren

A

BUN/Cr, K+

72
Q

should you combine an ACE + ARB or Aliskiren with ACE/ARB

A

nah

73
Q

a-adrenergic antagonists (& long or short acting)

A

long-acting: terazosin, doxazosin

short acting: prazosin

74
Q

what is common with a-blockers if they are not combined with a diuretic

A

fluid retention

75
Q

a-blocker MOA

A

a1-receptor antagonist = decreased arterial PSI by dilating resistance and capacitance vessels

76
Q

a-blockers indications

A

BPH (but now Tamsulosin&raquo_space;)
“medical expulsive therapy” for ureteral stones
HTN (less use, poor data)
prazosin - PTSD in combat veterans?

77
Q

ADRs for a-blockers (when used for BPH)

A 
*postural hypotension/dizziness (1st few doses >>)
drowsiness/fatigue
*nasal congestion/rhinitis 
retrograde ejaculation 
floppy iris syndrome
78
Q

non-selective B-blockers

A

propranolol
timolol
nadolol

79
Q

cautions when using nonselective B-blockers

A

COPD, asthma, raynauds pts

80
Q

selective B1-blockers

A

metoprolol

81
Q

tartrate vs succinate

A

tartrate - IR - dosed BID-TID

succinate - ER - dosed QD (used for HF)

82
Q

nonselective B-blockers with a1-blocking activity

A

carvedilol

labetalol

83
Q

selective b-blockers with increase NO release from endothelial cells

A

nebivolol

84
Q

b-blockers MOA

A

competitive inhibitors of catecholamines at B-receptors

85
Q

B1 receptors vs B2 receptors

A

B1- heart = increase HR/contractility/AV conduction

B2 - bronchial, peripheral vascular smooth muscle > heart muscle = vasodilation, bronchodilation

86
Q

indications for B-blockers

A

HTN + angina
HTN + a-fib
HTN + HFrEF

87
Q

additional uses for B-blockers

A

propranolol - infantile hemangiomas
migraines
essential tremor
pheo/hyperthyroidism

88
Q

when stopping B-blockers

A

taper over 1-2 weeks

can cause angina, AMI

89
Q

who else are B-blockers contraindicated in

A

pts with 2nd/3rd degree heart block, SSS, bradycardia <50 bpm

90
Q

important interaction of B-blocker

A

blunts effects of epi (EpiPen)

91
Q

b-blocker ADRs

A 
hyperkalemia
bradycardia
fatigue/exercise intolerance 
floppy iris syndrome 
bronchospasm
92
Q

b-blockers may mask/delay recovery from…

A

hypoglycemia (non-selective)

*careful in diabetics

93
Q

non-dhp ccbs

A

verapamil

diltiazem

94
Q

dhp ccbs (and short v long acting)

A

short acting: nifedipine

long acting: amlodipine

95
Q

CCB MOA

A

relax arterial smooth muscle, produce peripheral vasodilation via inhibiting L-type calcium channel

96
Q

where do DHP CCBs act primarily

A

in vascular smooth muscle to decrease PVR

97
Q

where do NON-DHP CCBs act primarily

A

effects cardiac contractility (verapamil>diltiazem)

less potent vasodilator

98
Q

indications for DHP CCBs

A

HTN
angina
raynauds

99
Q

indications for NON-DHP CCBs

A

cardiac arrhythmias

cluster HA prophylaxis - verapamil

100
Q

who should you not use NON-DHP CCBs in

A

2nd/3rd degree heart block
SSS
bradycardia <50
HF

101
Q

CCB class effect ADRs

A

peripheral edema, reflex tachycardia, HA, dizziness, flushing

102
Q

verapamil ADR

A

constipation

103
Q

nifedipine ADR

A

gingival hyperplasia

104
Q

central a-adrenergic agonists

A

clonidine

methyldopa

105
Q

a-agonist ADRs

A

dry mouth, sedation

HTN crisis if abrupt withdrawl

106
Q

direct vasodilators

A

hydralazine

minoxidil

107
Q

direct vasodilator MOA

A

relaxes arterial smooth muscle–> decreases PVR

108
Q

hydralazine indications

A
  • HTN
  • pre-eclampsia/eclampsia
  • HF (hydralazine + isosorbide dinitrate = BiDil)
109
Q

what should you combine direct vasodilators with and why

A

B-blocker or centrally-acting drug - minimizes reflex increase in HR/CO
diuretic - avoid Na, H20 retention

Pharmacology PaxFlan (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions