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PharmSci > Heart failure drugs > Flashcards

Heart failure drugs Flashcards

1
Q

What is heart failure?

A

HF is a progressive clinical syndrome that is an abnormality in the structure of function of the heart that impairs the ability of the ventricle to eject blood out

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2
Q

Does the heart meet metabolic demand in HF?

A

NO

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3
Q

Is your CO low or high in HF?

A

LOW

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4
Q

To compensate for HF, what systems does the body activate?

A

SNS & RAAS

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5
Q

What are the effects of SNS activation?

A

(+) ß-1–> increased CO, HR, contraction, & MAP

(+) alpha-1 –> increased VC & MAP

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6
Q

What are the effects of RAAS activation?

A

VC –> increased MAP
Aldosterone: increased Na+ & water reabsorption
increased blood vol, preload, FOC

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7
Q

In cardiomyocytes, __________ binds Ca2+ which results in a conformational change, exposing the actin-binding site on the myosin filament, thereby allowing for cross-bridge formation.

A

Troponin C

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8
Q

____ is critical for the contraction of all types of muscle cells.

A

Calcium

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9
Q

What is the MOA of Digoxin?

A

Inhibits the Na+/K+ ATPase pump on cardiac myocytes.

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10
Q

What is the effect of digoxin on intracellular Na+ levels?

A

increases [Na+]

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11
Q

What is the effect of digoxin on Ca2+ removal from the cell?

A

decreases (Ca2+ stays in the cell)

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12
Q

How does digoxin effect contraction?

A

increases (b/c more Calcium is in the SR and this increases the pumping ability of the heart)

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13
Q

Digoxin acts in a ________ manner.
A. Parasympathetic
B. Sympathetic

A

A

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14
Q

What is the effect of K+ on digoxin activity?

A

If you increase [K+], you DECREASE digoxin activity

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15
Q

Why does K+ effect digoxin activity?

A

Digoxin and K+ bind near the same site on the Na+/K+ ATPase pump.

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16
Q

Digoxin, at therapeutic doses, causes a ___________ effect allowing digoxin to slow the AV node. This is good for which type of patients?

A

vagomimetic

This is good for patients who have supraventricular tachycardias such as atrial fibrillation

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17
Q

What are 2 effects that digoxin has on baroreceptor reflex?

A
  1. turn down sensitivity to baroreceptor reflex

2. increases baroreceptor response (by decreasing constant activation & decreasing sensitivity)

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18
Q

How is digoxin cleared?

A

renally (mostly)

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19
Q

What is digoxin a substrate of?

A

Pgp

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20
Q

Does digoxin have good absorption from the GI tract?

A

YES!

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21
Q

What is digoxin’s half-life?

A

36 h

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22
Q

About how long does it take to get to steady state with digoxin?

A

about one week (LD is very important)

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23
Q

Does digoxin have a narrow or wide therapeutic range?

A

NARROW

high risk of toxicity

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24
Q

What are the adverse effects of digoxin?

A 
N/V
Vision disturbances (yellow/green)
AV nodal block
Ventricular arrhythmias
Fatigue
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25
Q

What are the drug interactions with digoxin?

A

Diuretics (hyper/hypokalemia)
BB & non-DHP CCBs (AV nodal block, decreased contractility)
Macrolide ABx (increased BA)
Amiodarone, proparenone (AA), verapamil, spirinolactone (increase digoxin levels)

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26
Q

Why does spironolactone interact with digoxin?

A

it is a Pgp inhibitor

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27
Q

How can spironolactone treat HF?

A

Spirinolactone helps decrease aldosterone’s affect on the heart and can be good in treating HF

28
Q

What is the role of aldosterone in HF?

A

in HF, aldosterone levels are significantly INCREASED (They cause cardiac remodeling & increased collagen deposits and fibrosis and
inhibits pumping effects of the heart: increases stiffness & thickness

29
Q

How does food affect spironolactone’s BA?

A

increases

30
Q

How is spironolactone metabolized?

A

hepatic ally metabolized to ACTIVE metabolites

31
Q

What is the half life of spironolactone’s metabolites?

A

Canrenone: 10-23 h

7-alpha-spirinolactone: 7-20 h

32
Q

What is the % of PB of spironolactone?

A

91-98%

33
Q

What are the adverse effects of spirinolactone?

A

N/V/D
Gynecomastia
Irregular menses
Impotence

34
Q

Drug interactions of spironolactone?

A

ACE-I and ARBs: hyperkalemia

Digoxin: hyperkalemia

35
Q

What drugs treat Acute Decompensated Heart Failure?

A

Milrinone

Nesiritide

36
Q

How does Milrinone work?

A

inhibits PDE-3 (prevents the breakdown of cAMP to AMP)

“inodilator” (increases FOC and VD)

37
Q

What is the onset of action of milrinone?

A

5-15 min

38
Q

What is the half-life of milrinone?

A

2.5 h (relatively short, used for acute situations)

39
Q

How is milrinone administered?

A

IV only

40
Q

How is milrinone cleared?

A

renally by active tubular secretion

41
Q

Milrinone has _____ and ______ effects.

A

cardiac & VSM

42
Q

What are the Adverse effects of Milrinone?

A

hypotension
arrhythmias
thrombocytopenia

43
Q

What is Nesiritide?

A

Recombinant B-type natriuretic peptide

44
Q

When is BNP released?

A

Released in response to volume overload

45
Q

What does Nesiritide cause?

A

Natriuresis, diuresis and vasodilation

46
Q

What is the MOA of Nesiritide?

A

Nesiritide binds NPR-A, which is a cell surface receptor with intrinsic guanylyl cyclase activity. Activation of this receptor increases intracellular cGMP levels in target tissues including smooth muscle cells. Increased cGMP mediates its effects including increased natriuresis and diuresis as well as vascular smooth muscle relaxation in both the venous and arterial systems. This results in a decrease in both preload and TPR.

47
Q

What is the onset of action of Nesiritide?

A

15 min

48
Q

What is the half-life of Nesiritide?

A

18 min

49
Q

When is Nesiritide used?

A

in ACUTE situations

50
Q

How is Nesiritide eliminated?

A
  1. Binding to cell surface receptor NPR-C and subsequent cellular internalization and degradation.
  2. Proteolytic cleavage by neutral endopeptidases
  3. Renal filtration
51
Q

What are the adverse effects of Nesiritide?

A

Hypotension

GI upset

52
Q

________ is part of the ACLS Guidelines for the treatment of cardiac arrest.

A

Vasopressin

53
Q

___________ is a non-adrenergic peripheral vasoconstrictor which also increases blood flow to the heart and brain.

A

Vasopressin

54
Q

What does vasopressin do?

A

Vasopressin binds to G protein coupled receptors resulting in peripheral vasoconstriction and water reabsorption in renal collecting duct.

55
Q

What is the VI receptor?

A

The V1 receptor is a Gq coupled receptor located on vascular smooth muscle.

56
Q

What happens in VSM when a Gq coupled receptor is activated?

A

vasoconstriction (VC)

57
Q

Vasopressin causes vasodilation of cerebral and coronary vessels. How/Why?

A

different location
different cells (endothelial cells)
Ca2+ –> eNOS –> increase NO –>VSM –> relaxation

58
Q

What is the half-life of vasopressin?

A

17-35 min

59
Q

Which drug is rapidly cleaved by proteases?

A

vasopressin

60
Q

What are the adverse effects of vasopressin?

A

N/V

Abdominal cramps

61
Q

The __________ is located on the basolateral side of the collecting duct. Activation of the Gs coupled receptor leads to activation of adenylyl cyclase. This results in increased cAMP levels and activity of PKA, which promotes the insertion of water channel-containing vesicles into the apical membrane as well as a decreased rate of endocytosis, increasing the permeability of water across the apical membrane.

A

V2 receptor

62
Q

What do ADH antagonists treat in HF?

A

hypervolemic hyponatremia

63
Q

What is aldosterone’s effect on the body?

A

increases Na+ and water reabsorption
secretes K+
increases bp

64
Q

What is vasopressin’s effect on the body?

A

increases water reabsorption
increases bp
VC

65
Q

What is spirinolactone’s effect on the body?

A

decreases sodium and water reabsorption
decreases fluid volume
decreases pressure
increases K+ reabsorption

PharmSci (12 decks)

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