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renal > antihypertensives > Flashcards

antihypertensives Flashcards

1
Q

hypertension systolic and diastolic

A

> 130/80

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2
Q

six types of diuretics

A 
carbonic anhydrase inhibitors
loop
thiazides
potassium sparing
vaptans
osmotic
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3
Q

acetazolamide is a

A

carbonic anhydrase inhibitor

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4
Q

carbonic anhydrase inhibitors MOA

A

inhibition of carbonic anhydrase in PCT leads to Na and HCO3 diuresis

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5
Q

indications for carbonic anhydrase inhibitors

A

acute glaucoma
altitude sickness
metabolic alkalosis
alkalinizes urine

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6
Q

carbonic anhydrase inhibitors adverse effects

A

sulfa allergies
hypokalemia
kidney stones
metabolic acidosis due to HCO3 loss

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7
Q

thiazides MOA

A

blocks NaCl cotransporter in distal tubule leading to increased sodium and water excretion

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8
Q

thiazides adverse effects

A

increase glucose, lipids, calcium, uric acid
hypOnatremia, hypokalemia
sulfa allergies

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9
Q

thiazide indications

A

HTN
peripheral edema
nephrogenic diabetes insipidus

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10
Q

furosemide is a

A

loop diuretic

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11
Q

loop diuretics MOA

A

inhibit NKCC2 symporter on TAL of LOH leading to dilute urine
(no reabsorption of Na, K Cl)

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12
Q

loop diuretics adverse effects

A

decreased electrolytes
ototoxicity
hypotension
sulfa allergy

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13
Q

loop diuretics indication

A

HTN
edema
hypercalcemia
hypermagnesemia

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14
Q

can be used for hypercalcemia

A

loop diuretics reduce reabsorption

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15
Q

K sparing agents MOA

A

aldosterone receptor antagonist in collecting duct increases Na and water excretion while concerning K and H

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16
Q

aldosterone antagonist K sparing diuretics indications

A

weak alone, use with thiazide/loop

hypokalemia
primary hyperaldosteronism
HTN
edema/ascites
CHF
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17
Q

Aldosterone antagonist K sparing diuretics adverse effects

A

hyperkalemia
gynecomastia
ED
Metabolic acidosis

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18
Q

ENaC K sparing diuretics adverse effects

A

kidney stones
hyperkalemia
metabolic acidosis

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19
Q

ENaC K sparing diuretics MOA

A

directly inhibit epithelial Na channel in collecting duct to increase NaCl and water loss

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20
Q

ENaC K sparing diuretics indications

A

HTN

CHF

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21
Q

ENaC blockers

A

triamterene

amiloride

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22
Q

vasopressin antagonists

A

tolvaptan

conivaptan

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23
Q

vasopressin antagonists’ MOA

A

block vasopressin type 2 receptor (V2) to prevent aquaporin insertion and decrease water reabsorption

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24
Q

Vasopressin antagonists’ adverse effects

A

hepatotoxicity
hypernatremia
thirst
(it is not really used)

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25
Q

vasopressin antagonists indication

A

hyponatremia (but they correct this too quickly)

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26
Q

mannitol is a(n)

A

osmotic agent

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27
Q

osmotic agents MOA

A

mannitol is a non-metabolized sugar which increases osmotic pressure of glomerular filtrate

draws more water into tubule to decrease reabsorption and increase diuresis

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28
Q

mannitol indications

A

elevated intracranial or intra-ocular pressure

urogenital irrigation

(not as an antiHTN)

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29
Q

mannitol adverse effects

A

hypotension
hypovolemia
pulmonary edema
vesicant >5% concentration

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30
Q

CCBs general MOA

A

bind to and block L-type calcium channels in smooth muscle cells leading to vasodilation and a drop in BP

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31
Q

DHP rx

A

amlodipine
nifedipine
nicardipine
clevidipine

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32
Q

DHPs primarily act on

A

vascular smooth muscles

amlodipine: arteries

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33
Q

Non DHP CCBs

A

verapamil

diltiazem

34
Q

Non DHP CCBs act on

A

the heart

verapamil ventricles

35
Q

what happens when the calcium channel is blocked?

A

Calcium cannot be released and the muscle cannot contract .

Ca is usually the signal for contraction

36
Q

preferred DHP in pregnancy

A

nicardipine

37
Q

Non DHPs _____ peripheral dilation, ______ HR, and ________ contractility

A

increase
decrease
decrease

38
Q

DHPs _____ peripheral dilation

A

increase

39
Q

adverse effects of Non-DHPs

A

bradycardia
heart block
gingival hyperplasia
constipation

40
Q

adverse effects of DHPs

A

headache
peripheral edema
flushing
reflex tachycardia

41
Q

indications for DHP CCBs

A

HTN
angina
Raynauds

42
Q

indications for Non-DHP CCBs

A

HTN
SVT
angina
cardiomyopathy

43
Q

contraindications for DHP CCBs

A

hypertrophic obstructive cardiomyopathy
stenotic valve defects
hypotension ACS

44
Q

contraindications for Non-DHP CCBs

A 
ACS
hypotension
bradycardia
conduction disorders
DO NOT USE WITH beta blockers
45
Q

do not use ______ with Non-DHPs because it will lead to _____

A

Beta blockers

severe bradycardia, AV block, decreased contractility

46
Q

5 classes of antihypertensives

A 
Diuretics
RAAS inhibitors 
CCBs
Adrenergic Agents
Direct-Acting Vasodilators
(Drugs Really Can Alter Diastole)
47
Q

RAAS inhibitors classes

A

Angiotensin-converting enzyme inhibitors (ACEis)

Angiotensin receptor blockers (ARBs)

48
Q

ACEi names end in ____

A

“pril”

49
Q

ARBs names end in

A

“sartan”

50
Q

ACEi MOA

A

blocks angiotensin converting enzyme in RAAS which does not allow angiotensin I to be converted to angiotensin II.

decreased angiotensin II
decreased aldosterone
vasodilation

51
Q

ACEis lead to a decrease in _____ and _____, which leads to ______

A

angiotensin II
aldosterone
vasodilation (lower BP)

52
Q

ACEi indications

A 
HTN
HFrEF
previous MI
CKD
diabetic nephropathy
53
Q

2 drug classes that are nephroprotective

A

ACEIs and ARBs

54
Q

ARBs MOA

A

block angiotensin II from binding to AT1 receptor which blocks the action of angiotensin II

vasodilation and lower BP

55
Q

ACEis and ARBs both _____ after load and _____ BP

A

decrease

lower

56
Q

angiotensin II causes

A

vasoconstriction (that is why is is targeted to treat HTN)

57
Q

aliskiren is a

A

direct renin inhibitor

58
Q

ACEi adverse effects

A

cough
angioedema
hypotension
hyperkalemia

59
Q

ARBs adverse effects

A

angioedema
hyperkalemia
decreased GFR

60
Q

direct renin inhibitor MOA

A

selectively blocks renin from activating RAAS which stops the whole process upstream so that vasoconstriction is decreased

decreased BP

61
Q

direct renin inhibitors adverse effects

A

diarrhea
hyperkalemia
teratogenicity

62
Q

direct renin inhibitors contraindications

A

pregnancy
if taking ACEs and ARBs (hyperkalemia)
DM

63
Q

ACEI/ARBs contraindications

A

pregnancy
aortic stenosis
renal artery stenosis

64
Q

do not combine ____ and ACEI/ARBs

A

direct renin inhibitors

65
Q

initial HTN treatment for a diabetic patient

A

ACEIs or ARBs

66
Q

increase in bradykinin concentration can lead to

A

dry cough

bradykinin mediated angioedema

67
Q

bradykinin is increased with use of what rx

A

ACEi

68
Q

bradykinin

A

inflammatory marker that leads to vasodilation

69
Q

chronotropic

A

affects HR

70
Q

inotropic

A

affects contractility

71
Q

alpha 1 blockers

A

doxazosin
prazosin
terazoin

72
Q

a1 blockers MOA

A

block a1 receptor on vascular smooth muscle to cause vasodilation

73
Q

a1 blockers adverse effects

A

orthostatic hypotension
dizziness
nausea

74
Q

prazosin indication

A

HTN

75
Q

terazosin/doxazosin indication

A

BPH

HTN

76
Q

A2 agonists

A

methyldopa

clonidine

77
Q

a2 agonists MOA

A

agonize A2 receptors to decrease vasoconstriction and lower BP

78
Q

direct vasodilators

A

hydralazine

minoxidil

79
Q

direct vasodilators MOA

A

direct relaxation of vascular smooth muscles to increase vasodilation and lower BP

80
Q

direct vasodilators adverse effects

A

rebound tachycardia

renal (17 decks)

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