Brainscape's Knowledge GenomeTM

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


See full index

Pharm I ( Melicia) > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Primary signs/sxs of HF

A

tachycardia, decreased exercise tolerance, SOB, cardiomegaly, peripheral/pulmonary edema

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

Compensatory responses in HF

A

increased SNS activity, increased preload, vasoconstriction, ventricular hypertrophy/remodeling

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

What are the 2 goals of treatment of HF

A
  • reduce sxs and slow progression as much as possible

- manage acute episodes of decompensated failure

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

Pharmacological tx for stage C HF with reduced EF?

A

Renin-Angiotension System Inhibition with ACE-I or ARB or ARNI

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

ARNIs should not be given to pts who…

A

are taking an ACE-I

those with hx of angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ivabradine can be beneficial to which pts?

A

Can reduce HF hospitalizations for pts with symptomatic stable chronic HFrEF who are receiving max dose of BB and are in NSR

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

What is recommended in additional to standard HF therapy in African American pts?

A

venodilator: hydralazine Isosorbide Dinitrate

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

MOA of Ivabradine

A

prolongs diastolic time by selectively and specifically inhibiting the Icurrent within the HCN channel, reducing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Side effects of Ivabradine

A

dizziness, fatigue

less common: increase BP, visual light disturbances, Afib

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

contraindications for Ivabradine

A

acute decompensated HF, BO <90/50, sick sinus syndrome, AA block, severe hepatic impairment, PPM dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Avoid use of Ivabradine with…

A

strong CYP3A4 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define systolic dysfunction

A

reduced mechanical pumping action and reduced EF

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

Define diastolic dysfunction

A

stiffening and loss of adequate relaxation —> reduction in filling and CO (EF may be norm)

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

What are the 4 stages in the ACC/AHA heart failure staging system?

A

Stage A: Pt at high risk for developing HF

Stage B: Pt with structural heart disease but no HF

Stage C: Pt with structural heart disease + current or hx of HF sxs

Stage D: refractory HF requiring specialized interventions

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

Therapies used in chronic systolic HF

A

diuretics, aldosterone antagonist, ACE-I, ARBs, BB, cardiac glycosides, vasodilators, resynchronization/CCV

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

Therapies used in acute HF

A

diuretics, vasodilators, beta agonists, bipyridines, natriuretic peptide, LVAD

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

What lab marker can be used to predict the prognosis and classification of HF?

A

BNP

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

Na/K ATPase inhibitors- example? MOA?

A

Digoxin

increases Ca, increase cardiac contractility (Chronic HF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Renal sodium transporter inhibitor- example? MOA?

A

Furosemide, Spironolactone, other diuretics

reduce preload and afterload (acute and chronic HF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ACE-I: example? MOA?

A

Lisinopril

reduce preload and afterload, reduce remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vasodilators: example? MOA?

A

Nitroprusside, Nitroglycerine

reduce preload and afterload
acute HF

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

Phosphodiesterase inhibitors: example? MOA?

A

Milrinone

vasodilation, increase contractility (acute HF)

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

Natriuretic peptide: example? MOA?

A

Nesiritide

vasodilation reduces preload and afterload; some diuretic effect (acute HF)

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

HCN:example? MOA?

A

Ivabradine

slows HR

(chronic stable worsening HF)

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

Where in the nephron does Furosemide act?

A

loop diuretic

decreases NaCl and KCl reabsorption in the thick ascending loop of henle

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

Loop diuretic (Furosemide) toxicities?

A

hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity

avoid in those with sulfa allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What will happen if you give a higher dose of Furosemide than what is included in the usual range (20-160mg)?

A

it is not likely that there will be an additional response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

HCTZ MOA?

A

decreases NaCL reabsorption in the distal convoluted tubule

same effect Furosemide but not as strong

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

When should you prescribe HCTZ?

A

in mild chronic HF, mild-mod HTN, hypercalciuria

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

HCTZ toxicities? contraindications?

A

hyponatremia, hypokalemia, hyperglycemia, hyperurecemia, hyperlipidemia

sulfa allergy

31
Q

What should you monitor in patients on HCTZ?

A

glucose, uric acid, electrolytes

32
Q

Name an Aldosterone Antagonist. MOA?

A

Spironolactone

blocks aldosterone receptors in collecting tubules of nephron -> increases Na and water excretion, reduces remodeling, reduces mortality

33
Q

When should you use an Aldosterone antagonist (Spironolactone)?

A

in chronic HF

also: aldosteronism, HTN

Really good bc it reduces remodeling

34
Q

Aldosterone Antagonist toxicities?

A

hyperkalemia, antiandrogen actions (i.e gynecomastia), renal toxicity

35
Q

How can you reduce the risk for hyperkalemia with Aldosterone Antagonists?

A

Start slow and make sure they have a Cr clearance so that the drug can be cleared

Avoid K+ supplements, avoid foods high in K+, avoid NSAIDS

monitor Cr

~need to give this drug carefully but can be very beneficial

36
Q

Effects of ACE-I

A

arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling

37
Q

Clinical applications for ACE-I?

A

Chronic HF, HTN, diabetic renal disease

38
Q

ACE-I side effects?

A

cough, hyperkalemia, angioedema

Avoid use with: other angiotensin antagonist

39
Q

When should you use an ARB? side effects?

A

When pt can’t tolerate ACE-I

hyperkalemia, angioedema

40
Q

Name a ANRi (Angiotensin Receptor Naprilosin Inhibitor)

A

Savubitril/valsartan (Entresto)

41
Q

What should you discontinue before starting pt on ANRi?

A

ACE-I (at least 36 hrs before starting)

42
Q

BB example? MOA?

A

Carvedilol

blocks B1 receptors and alpha1 receptors –> slows HR, reduces BP

43
Q

When should you use a BB?

A

in chronic HF, slows progression

44
Q

BB side effects?

A

bronchospasm, bradycardia, AV block, acute cardiac decompensation

45
Q

Name 3 Vasodilators

A

Veno: Isosorbide Dintrate, Hydralazine Isosorbide Dinitrate,

Arterial: Hydralazine

46
Q

Isosorbide dinitrate MOA?

A

releases nitric oxide- activates guanylyl cyclase -> venodilation: reduces preload and ventricular stretch

47
Q

Side effects of isosorbide dinitrate?

A

postural hypotension, tachycardia, HA

48
Q

Effect of Hydralazine?

A

reduces BP and afterload: results in increased CO

49
Q

Side effects of Hydralazine?

A

tachycardia, fluid retention, lupus like syndrome

50
Q

What class of drug is Nitroprusside in? MOA?

A

Vasodilator

rapid powerful vasodilation reduces preload and afterload

51
Q

When should you use Nitroprusside?

A

acute severe decompensated failure

52
Q

Nitroprusside toxicities?

A

excessive hypotension, thiocyanate and cyanide toxicity

53
Q

Can you give Nitroprusside over several days?

A

NO! Its metabolism causes cyanide

54
Q

Name a cardiac glycoside, MOA?

A

Digoxin

Na/KATPase inhibition results in reduced Ca expulsion and increased Ca stored in SR –>

increases cardiac contractility, cardiac parasympathomimetic effect??

55
Q

When can you use Digoxin?

A

chronic sxs HF

rapid ventricular rate in AFib

56
Q

Side effects of Digoxin?

A

N/V/D

cardiac arrhythmias

57
Q

Digoxin dose should be lowered in which pts?

A

elderly, those with low lean body mass, impaired renal func.

58
Q

Effects of Digoxin on ECG: therapeutic dose, toxic dose?

A

increases PR interval, decreased QT interval

tachycardia, fibrillation, arrest at really high dose

59
Q

Name 2 Beta Adrenoceptor Agonists

A

Dobutamine, Dopamine

60
Q

Dobutamine MOA?

A

beta1 selective agonist–> increases cardiac contractility

only use in acute HF

61
Q

Dobutamine toxicities?

A

arrhythmias

62
Q

Dopamine MOA?

A

dopamine receptor agonist –> increased renal blood flow, higher doses increase cardiac force and BP

63
Q

When can you use Dopamine?

A

Acute decompensated HF and shock

64
Q

Dopamine toxicities?

A

arrhythmias

additive effect with sympathomimetics

65
Q

Name a bipyridine, MOA?

A

inamrinon, milrinone

phosophodiesterase type 3 inhibitors- decreased cAMP breakdown—> vasodilators, lower PVR and increased cardiac contractility

66
Q

When can you use bipyridines? toxicities?

A

acute decompensated HF

( increases mortality in chronic HF)

arrhythmia

67
Q

Name a natriuretic peptide, MOA?

A

Nesiritide

activates BNP receptors, increases cZGMP–> vasofilation and diuresis

68
Q

When can use a natriuretic peptide? toxicities?

A

acute decompensated failure

renal damage, hypotension, may increase mortality

69
Q

Ivabradine is a…

A

HCN I-f inhibitor

70
Q

When can you use Ivabradine?

A

when pt has sxs of HF that are stable

normal HR, taking a BB at highest dose tolerated

71
Q

How should you treat class A HF?

A

No sxs but risk factors:

Treat obesity, HTN, DM, hyperlipidemia, etc.

72
Q

How should you treat class B HF?

A

sxs with severe exercise:

diuretic, ACEI/ARB, BB

73
Q

How should you treat class C HF?

A

sxs with marked or mild exercise:

diuretic, ACEI/ARB/BB +

aldosterone antagonist, Digoxin, CRT, hydralazine/nitrate

74
Q

How should you treat class D HF?

A

drugs from class A-C

transplant, LVAD

Pharm I ( Melicia) (18 decks)

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