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SPR2015_Week2 > Diuretics and RAAS Antagonists Use in HF > Flashcards

Diuretics and RAAS Antagonists Use in HF Flashcards

1
Q

what is Baroreceptor response

A

incr sympathetic discharge

short term

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2
Q

what is the RAAS response

A

incr renin release

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3
Q

Goals of heart failure management with pharmacotherapy (3)

A

1) reduce congestion with diuretics
2) modulate neurohormonal activation (RAAS antag + Beta blocker)
3) improve flow with vasodilations

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4
Q

regardless of HF Type, ___

A

ALWAYS CONTROL VOLUME FIRST WITH DIURESIS

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5
Q

Chronic HFrEF

A

1) beta blocker
2) ACE inhibitor/ARB
3) aldosterone antagonist
4) Hydralazine/ISDN
5) +/- digoxin
6) ICD/CRT

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6
Q

Chronic HFpEF

A

1) control risk factor (DM, HTN, obesity)

2) control volume

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7
Q

Acute HFrEF

A

1) IV diuresis
2) nitrate (if BP allow)
3) CPAP/BiPAP (if SOB)
4) Pressors (VERY LOW CO, SHOCK)

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8
Q

Acute HFpEF

A

1) IV diuresis
2) nitrates (if BP allows)
3) CPAP/BiPAP

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9
Q

first thing with chronic HFpEF, acute HFrEF or HFpEF

A

IV diuresis/volume control

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10
Q

purpose of diuretics

A

1) Na/H2O excretion
2) decr intravascu fluid volume
3) decr venous congestion
4) decr dyspnea/edema

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11
Q

effect of diuretics of LVEDP vs. SV curve

A

shift a given point to the left but staying on the same curve line

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12
Q

Diuretics use

A

USE FIRST AS NEEDED TO REDUCE congestion

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13
Q

Purpose of diuretics

A

lower preload, decr Na/H2O retention

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14
Q

which type of diuretics preferred?

A

loop because of efficacy

can augment with thiazide diuretic

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15
Q

diuretics can be used ___ and ___

A

chronically and acutely

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16
Q

When do you use ACEI’s

A

during or after optimization of diuretic therapy

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17
Q

effect of ACEI’s?

A

1) vasodilation
2) decr aldosterone activation
3) antiremodeling effects

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18
Q

when do you use aldosterone antagonists?

A

ADDED for LVEF <30% with ACEI/ARB and B-blocker therapy

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19
Q

K+ effect of aldosterone antagonist

A

1) monitor serum K+ 30 mL/min (K+ sparing)

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20
Q

function of aldosterone antagonist

A

1) antiremodeling action 2) additional Na+ loss at kidney

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21
Q

2 names of aldosterone antagonists

A

1) spironolactone - gynecomastia

2) eplernone

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22
Q

where do most diuretics exert their effects?

A

at luminal (urine surface) of renal cells

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23
Q

What is mechanism of thiazide and furosemide?

A

interact with membrane transport proteins

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24
Q

which diuretics interact with membrane transport proteins?

A

thiazide

furosemide

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25
Q

what is mechanism of spironolactone

A

interact with hormone receptor

26
Q

which diuretic interacts with hormone receptors

A

spironolactone

27
Q

how is Na+ level controlled?

A

active transport via Na+/K+ ATPase at interstitial (BLOOD) surface

in kidney, Na+ reabsoprtion

28
Q

how do diureitcs affect Na+ levels

A

1) decr Na+ reabsoprtion

2) Na+ and H2O into urine

29
Q

mechanism of loop diuretics

A

1) inhib NaCl transport in thick ascending limb across lumen-urine
2) decr gradient to pump K+ out
3) incr Mg2+/Ca2+ excretion

30
Q

what is unique about when you can use loop diuretics?

A

YOU CAN USE ON RENAL FAILURE PATIENTS

31
Q

pharmacokinetics of loop diuretics

A

variable bioavaiability with furosemide

fast IV

32
Q

how are loop diuretics excreted?

A

glomerular filtration

renal secretion

33
Q

negative of filtration of loop diuretics?

A

same transporter as uric acid –> hyperuricemia

34
Q

which loop diuretic has shortest half life and which has longest?

A

furosemide = shortest

bumetanide = longest

35
Q

when do you use loop diuretics

A

HF patients with volume overload

36
Q

how are loop diuretics enhanced?

A

with salt restriction

37
Q

what happens if furosemie cannot be used?

A

1) incr dose
2) switch to bumetanide/torsemide (more reliable + longer duration)
3) IV administration
4) ethacrynic acid for non-sulfa form

38
Q

what are the mechanisms in HF patients with decr diuretic response

A

1) decr drug delivery to kidney via decr renal blood flow

2) low perfusion ACTIVATES RAAS AND SYMP NS

39
Q

when do you get refractory edema side effect of loop diuretics?

A

when you pair with thiazide

40
Q

how does loop + thiazide cause refractory edema?

A

1) block distal tubule Na+ reabs

2) counter loop induced incr in Na+ delivery

41
Q

what can you do to treat patients with refractory edema

A

1) give them aldosterone antagonist to incr diuresis and incr K+ sparing

42
Q

side effects of loop diuretics

A

1) hypokalemic metabolic alkalosis (b/c incr K+ and H+ excretion)
2) hyperuricemia - gout

43
Q

mechanism of thiazide diuretics

A

1) inhib Na+/Cl- cotransporter, incr urine excr of NaCl

44
Q

how effective are thiazides?

A

less than loops because only 5-10% of filtered Na+ is NORMALLY reabsorbed here

45
Q

difference btwn thaizides and loops in level of Ca2+

A

Thiazides - incr reabs of Ca2+

Loop - decr Ca2+

46
Q

compare use of thiazide and loops for CHF

A

higher dose for thiazide in HTN

usu need loops for CHF

47
Q

side effects of thiazides

A

1) hypokalemia –> ectopic pacemaker
2) hyperglycemia
3) hyperuricemia –> gout

48
Q

amount of diuresis for K+ sparing diuretics?

A

mild diuresis alone

49
Q

difference btwn mechanism of K+ sparing vs. K+ wasting?

A

K+ sparing –> block collecting tubule Na+ reabs receptor –> decr K+ excretion

K+ wasting –> block proximal Na+ reabs, incr K+ excretion

50
Q

mechanism of spironolactone

A

competitive antagonist at aldosterone receptor

51
Q

mechanism of triamterene/amiloride

A

direct block Na+ in collecting duct lumen, decr Na+ reabs

NO UTILITY IN HF

52
Q

what is a key criteria before giving patient K+ sparing diuretic?

A

make sure kidney works well (or else hyperkalemia)

53
Q

why are aldosterone antag (K+ sparing) used in HF?

A

block aldo receptors on heart –> RAAS antagonist

anti-remodeling

incr K+

54
Q

side effects of aldosterone antag

A

1) hyperkalemia

2) gynecomastia (block androgen receptor)

55
Q

factors that incr risk of hyperkalemia with aldosterone antag

A

1) incr age
2) renal failure
3) higher dose
4) combined ACEI + ARB
5) NSAID

56
Q

what in common amongst use of ACEI/ARB, B blocker, Aldosterone receptor blocker

A

anti-remodeling, decr fibrosis/apoptosis

57
Q

mechanism of ACE inhibitor

A

decr myocardial hypertrophy and remodeling

58
Q

pharmacokinetics of ACE inhibitor

A

1) absorb orally
2) prodrug convert to active metabolity in liver
3) elim by kidney
4) once-daily

59
Q

side effects of ACE inhibitor

A

cough
renal dysfunction
hypotension
hyperkalemia

teratogenic

60
Q

advantage of ARB over ACEI

A

more complete inhib of Ang II

no cough

61
Q

disadvantage of ARB over ACEI

A

loss of bradykinin vasodilation

62
Q

side effects of ARB

A

ACEI without cough

contraindicate in pregnancy

SPR2015_Week2 (19 decks)

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