Htn Drugs

Front 1

What is first line agent for htn?

Back 1

thiazide diuretic

Front 2

What are the classes of diuretics?

Back 2

thiazide, loop, K sparing, and aldosterone antagonist

Front 3

What is the weakest diuretic?

Back 3

K sparing

Front 4

Why do you see drop in BP when first start diuretic?

Back 4

diuresis

Front 5

Why do you see drop in BP after prolonged diuretic tx?

Back 5

peripheral vascular resistance decreases

Front 6

What aditional actions do thiazide diuretics have?

Back 6

mobilize Na and water from arteriolar walls, relaxes the lumen and increases diameter, peripheral vascular resistance drops
may cause direct relaxation of vascular smooth muscle

Front 7

What diuretic should be used if diuresis is required to rx edema, such as in heart failure?

Back 7

loop

Front 8

When should diuretics be dosed?

Back 8

morning if daily
morning and afternood if BID

Front 9

Do diuretics lower BP by extrarenal or intrarenal mechanisms?

Back 9

extrarenal

Front 10

What is more potent HCTZ or chlorthalidone?

Back 10

chlorthalidone 1.5-2x

Front 11

What are SE of thiazides?

Back 11

hypokalemia, hypomagnesemia, hypercalcemia, hyperuricemia, hyperglycemia, dyslipidemia, and sexual dysfunction

Front 12

What are SE of loop?

Back 12

same as thiazide, but hypocalcemia

Front 13

What should be used if pt develops gout when taking diuretic?

Back 13

allopurinol(Zyloprim)

Front 14

What is main SE of K sparing diuretics?

Back 14

hyperkalemia

Front 15

Which K sparing diuretic causes the most hyperkalemia?

Back 15

aldosterone antagonist: eplerenone(Inspra)

Front 16

When is eplerenone CI?

Back 16

impaired kidney function and type 2 DM

Front 17

Whis is a se of spironolactone?

Back 17

gynecomastia

Front 18

What drug should diuretic not be given with?

Back 18

lithium, may cause toxicity

Front 19

What is MOA of eplerenone (Inspra)?

Back 19

aldosterone receptor antagonist, block aldosterone binding to receptor, increases serum aldosterone and plasma renin

Front 20

What is MOA of Thiazides?

Back 20

inhibit reabsorbtion of Cl and Na in the cortical thick ascending limp of the loop of henle and early cortical tubules

Front 21

What is MOA of furosemide and ethacrynic acid?

Back 21

loop diuretic: inhibits reabsorption of Na and Cl in proximal and distal tubules, and loop of Henle

Front 22

What is MOA of bumetanide?

Back 22

loop diuretic:more chloruretic than natriuretic effect, action in proximal tubule, does not act on distal

Front 23

What is MOA of torsemide?

Back 23

loop diuretic: acts in lumen of thick ascending portion of loop of Henle, inhibits Na/K/2Cl carrier system

Front 24

What is MOA of spironolactone?

Back 24

competitive inhibitor of aldosterone

Front 25

What is MOA of K sparing diuretics?

Back 25

inhibit Na reabsorption induced by aldosterone and inhibit basal Na reabsorption

Front 26

What do ACE inhibitors do?

Back 26

block ACE inhibiting the conversion of Ang1 to Ang2
vasodilation and decrease in aldosterone occur

Front 27

What is the only ACEI that can't be dosed once daily?

Back 27

captopril (Capoten)

Front 28

What is the only ACEI that absorption is decreased when given with food?

Back 28

captopril (Capoten)

Front 29

What is SE of ACEI?

Back 29

hyperkalemia, acute kidney failure (rare), angioedema, dry cough, lithium toxicity

Front 30

When should K levels be checked when starting and ACEI?

Back 30

within 4 weeks

Front 31

Why does ACEI cause a cough?

Back 31

inhibition of bradykinin breakdown

Front 32

When are ACEI an ARBs CI?

Back 32

pregnancy

Front 33

What might occur if use ACEI with K sparing diuretic?

Back 33

hyperkalemia

Front 34

What is sulfhydryl containing ACEI?

Back 34

captopril

Front 35

What is phosphorus containing ACEI?

Back 35

fosinopril (Monopril)

Front 36

What are all other ACEI besides captopril and fosinopril?

Back 36

dicarbocyl containing

Front 37

What is MOA of ACEI?

Back 37

prevent conversion of Ang 1 to Ang 2 by inhibiting ACE

Front 38

What is MOA of ARBs?

Back 38

directly block the angiotensin II receptor subtype I receptor

Front 39

What do ACEI block that ARBs dont?

Back 39

bradykinin, get beneficial effects from not blocking it

Front 40

What drug class had a lower occurrence of recurrent strokes ARBs or CCBs?

Back 40

ARBs

Front 41

What kind of dose response curves does ARBs have?

Back 41

flat, increasing dose doesn't give much benefit

Front 42

How are most ARBs dosed?

Back 42

daily

Front 43

Which ARBs may require BID dosing?

Back 43

candesartan (Atacand), eprosartan (Teveten), losartan (Cozaar), valsartan (Diovan)

Front 44

Which antihypertensives have the lowest SE?

Back 44

ARBs

Front 45

What are SE of ARBs?

Back 45

renal insufficiency, hyperkalemia, orthostatic hypotension, angioedema is less likely to occur compared to ACEI

Front 46

Are dihydropyridines or nondihydropyridines more cardioprotective?

Back 46

nondihydropyridines

Front 47

What should be used in long acting isolated systolic hypertension?

Back 47

long acting dihydropyridine CCB

Front 48

What is MOA of CCB?

Back 48

inhibit influx of calcium across cell membrane by blocking high voltage channel (L type)

Front 49

What are the only CCB that dont have negative inotropic effects?

Back 49

amlodipine and felodipine

Front 50

What is the short acting CCB?

Back 50

nifedipine immediate release, not approved for HTN tx, more CV adverse effects

Front 51

What are SE of nondihydropyridine CCB?

Back 51

bradycardia, AV block, anorexia, nausea, peripheral edema, hypotension

Front 52

What is DI for nondihydropyridine CCB?

Back 52

CYP 3A4 inhibitor

Front 53

What is problem when giving nondihydropyridine and BB?

Back 53

increased risk of heart block

Front 54

How does BB reduce cardiac output?

Back 54

negative chronotropic and inotropic cardiac effects

Front 55

What is BB MOA?

Back 55

beta adrenergic receptor blocking agents, some block B1 only (cardioselective, BEAM), some block B1 and B2

inhibit B adrenoceptors and release of renin

Front 56

What are the cardioselective BB?

Back 56

betaxolol, bisoprolol, esmolol, atenolol, acebutolol, metoprolol

more selectivity for B1 receptors than B2

Front 57

Which BB are preferred for HTN cardioselective or nonselective?

Back 57

cardioselective

Front 58

What are the ISA BB?

Back 58

carteolol(Cartrol), pindolol (Visken), acebutolol (Sectral), penbutolol(Levatol)

Front 59

What is SE of ISA BB?

Back 59

resting heart rate, cardiac output, and peripheral blood flow not reduced

Front 60

What BB are renally excreted?

Back 60

atenolol and nadolol

Front 61

What BB undergo 1st pass metabolism?

Back 61

propranolol and metoprolol

Front 62

What is the most lipophilic BB?

Back 62

propranolol

Front 63

What is the least lipophilic BB?

Back 63

atenolol

Front 64

What are SE of BB?

Back 64

bradycardia, AV conduction abnormalities, acute heart failure

Front 65

What can happen if stop BB abruptly?

Back 65

unstable angina, MI, or death
rebound HTN

Front 66

How should BB be d/c?

Back 66

tapered over 1-2 weeks

Front 67

What is alpha 1 blocker MOA?

Back 67

inhibit uptake of catecholamines in smooth muscle cells resulting in vasodilation and BP lowering

Front 68

Are alpha 1 blockers used as monotherapy?

Back 68

no, only as an addition to primary antihypertensive agents

Front 69

What is SE of alpha 1 blockers?

Back 69

"first dose" phenomenon characterized by transient dizziness or faintness, palpitations, and syncope within 1-3 hours of first dose, this is accumpanied by orthostatic hypotension

Front 70

What MOA does Aliskiren have??

Back 70

direct renin inhibitor (blocks RAAS at point of activation)

Front 71

When is Aliskiren CI?

Back 71

pregnancy

Front 72

What are SE of aliskiren?

Back 72

angioedema, increased creatinine and serum K

Front 73

What is MOA of alpha 2 agonists?

Back 73

stimulates alpha 2 adrenergic receptors in the brain reducing sympathetic outflow from vasomotor center in brain and increases vagal tone

Front 74

What are SE of alpha 2 agonists?

Back 74

sodium and water retention, orthostatic hypotension

Front 75

What additional SE does clonidine have?

Back 75

anticholinergic SE (sedation, dry mouth, constipation, urinary retention, blurred vision)

Front 76

Should clonidine be used for chronic antihypertensive therapy in the elderly?

Back 76

no

Front 77

What can abrupt cessation of central alpha 2 agonist lead to?

Back 77

rebound hypertension
using BB can enhance this effect

Front 78

What are severe SE of methyldopa?

Back 78

hepatitis and hemolytic anemia

Front 79

What is MOA of reserpine?

Back 79

depletes NE from sympathetic nerve endings and blocks transport or NE to storage granules
also depletes catecholamines in brain and myocardium

Front 80

How long before see max effect from reserpine?

Back 80

2-6 weeks

Front 81

When giving reserpine, what should always be given with it?

Back 81

diuretic (thiazide)

Front 82

What is a SE that reserpine may have?

Back 82

depression

Front 83

What are the direct arterial vasodilators?

Back 83

hydralazine and minoxidil

Front 84

When using a direct arterial vasodilator what should always be given with it?

Back 84

diuretic and BB

Front 85

What is a SE unique to hydralazine?

Back 85

lupus like syndrome
slow acetylators especially prone to develop

Front 86

How do you avoid lupus like syndrome with hydralazine?

Back 86

use less than 200mg

Front 87

What is a SE of minoxidil?

Back 87

hirsutism (hypertrichosis)

Front 88

What diuretic should be used with minoxidil?

Back 88

loop

Front 89

What CCB is ultrashort acting, IV, used for hypertensive crisis?

Back 89

clevidipine (Cleviprex)