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Cardio > CHF Pharm > Flashcards

CHF Pharm Flashcards

1
Q

According to ACC/AHA guidelines, a patient who is stage A can be characterized by what?

A

AT RISK for CHF

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2
Q

According to ACC/AHA guidelines, a patient who is stage B can be characterized by what?

A

Low EF but no symptoms

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3
Q

According to ACC/AHA guidelines, a patient who is stage C can be characterized by what?

A

edema and dyspnea

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4
Q

According to ACC/AHA guidelines, a patient who is stage D can be characterized by what?

A

advanced heart failure

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5
Q

How do you treat a stage A CHF patient?

A

1) Preventive Measures (treating hypertension, dyslipidemia, diabetes, stopping smoking and alcohol intake)
2) ACE inhibitor or ARB

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6
Q

What do you add on to the treatment of a stage B CHF patient?

A

Other than preventative measures and ACEI/ARB, you use a beta blocker

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7
Q

What do you add on to the treatment of a stage C CHF patient?

A

Preventative measures, ACEI/ARB, Beta blocker and add on diuretic/digoxin/spironolactone

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8
Q

How do you treat a stage D CHF patient?

A

you need to give IV inotropes and transplant along with the other therapy

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9
Q

What is the MOA of ACE inhibitors?

A

block angiotensin I to angiotensin II conversion in the lung

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10
Q

Which ACE inhibitors are NOT prodrugs?

A

captopril and lisinopril

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11
Q

What is the MOA of ARBs?

A

block AT1 receptors to induce vasodilation and increase Na+ and water excretion

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12
Q

What is the ending to ARBs?

A

-tans (ex. losartan)

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13
Q

What is the MOA of aliskiren?

A

directly inhibits the protease activity of renin

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14
Q

Renin is released from the kidney to act on what chemical? What is this released from?

A

REnin is released from the kidney and converts angiotensinogen (from liver) to angiotensin

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15
Q

ACE inhibitors lead to what effects?

A
  • Decrease TRP (prevent vasoconstriction)
  • Decrease aldosterone (natriuresis, loss of Na and fluids)
  • Increase Bradykinin levels
  • Increase prostaglandin production (increased vasorelaxation)
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16
Q

What are the specs of ACE inhibitor use. (who do these work on, who do they not work on, contraindications)

A
  • Not good for African Americans
  • Not good for low-renin HTN
  • Decreases mortality post MI
  • Preserves renal function in diabetics
  • Little effect on lipids/sexual function
  • FETOTOXIC
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17
Q

What are the 2 most common adverse effects of ACE inhibitors?

A

1) first dose HTN

2) Na+ depletion

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18
Q

What are the other common adverse effects of ACE inhibitors?

A
  • Dry cough
  • Hyperkalemia
  • Angioedema (allergic skin/mucosa disease)
  • Renal insufficiency
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19
Q

ARBs have basically the same effects of ACE inhibitors, except they do not have what side effect?

A

dry cough

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20
Q

What are the side effects of ARBs?

A
  • 1st does hypotension
  • Hyperkalemia
  • Hepatic dysfunciton
  • Fetotoxicity
  • Spruelike enteropathy (from olmesartan)
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21
Q

Aliskiren has DDIs with what drugs?

A

drugs that inhibit p-glycoprotein (because aliskiren does too): erythromycin, amiodarone, etc.

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22
Q

What are the mitogenic effects of angiotensin II that ACE inhibitors and ARBs inhibit?

A

1) Hypertrophy of cardiac myocytes
2) Hypertrophy of vascular SM
3) Cardiac and vascular fibrosis (remodeling)
4) Atherosclerosis

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23
Q

Which drug has the phenomenon of aldosterone “escape”?

A

ACE inhibitors, over time, can no longer prevent the synthesis of aldosterone synthesis and this begins to increase

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24
Q

When would you use an ARB over an ACE inhibitor?

A

if you cannot tolerote an ACE inhibitor (due to dry cough, etc.)

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25
Q

Why were beta-blockers once contraindicated in CHF therapy?

A

becasue beta activation increases inotrophy needed when you have CHF

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26
Q

Beta blockers mainly treat CHF by attenuating the deleterious effects of chronic high levels of what?

A

norepinephrine and epinephrine

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27
Q

How do chronic high levels of NE and Epinephrine influence CHF?

A
  • Beta receptor down regulation
  • Arrhythmias (cause of death in CHF)
  • Increased myocardial oxygen consumption (ischemia)
  • Myocyte apoptosis followed by fibrosis
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28
Q

What are the short-term hemodynamic effects of beta blockers in CHF?

A

reduced CO and BP (may see initial worsening of symptoms before they get better)

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29
Q

What are the long-term hemodynamic effects of beta blockers in CHF?

A

increased CO, decreased LVEDP

30
Q

When do you want to start beta blockers?

A

early in CHF to slow disease progression

31
Q

List the beta blockers approved for CHF treatment.

A

Metoprolol
Crvedilol
Bisoprolol

32
Q

What are the major molecular effects of beta blockers in CHF?

A

1) reverse desensitization of beta receptors
2) increase receptor number
3) restore fast signaling modes (contractility) over slow signaling modes (gene expression)

33
Q

What is unique about the chemical structure of digitalis?

A

CARDIAC GLYCOSIDE

  • Steroid nucleus
  • Unsaturated lactone ring
  • Glycoside residues
34
Q

What are the sources of digitalis?

A

plants and toad venom

35
Q

Why is digoxin almost exclusively used now?

A
  • Convenient pharmacokinetics
  • Multiple ROA
  • Assay for measurements of serum levels
36
Q

What is the MOA of digoxin?

A

Increased intracellular availability of calcium for contractile apparatus via inhibition of sodium potassium pump (increase intracellular Na+. decrease intracellular K+)

37
Q

What does digoxin do to the pressure-volume curve?

A

shifts the curve upward and to the left

38
Q

Because digoxin is excreted unchanged by the kidney, how should you alter the dose in renal disease?

A

reduce it!

39
Q

How do you monitor the therapeutic action of digoxin?

A

plasma concentrations correlate roughly with theraapeutic effect and toxicity

40
Q

What are the adverse effects of digoxin?

A
  • Atrial and ventricular arrhythmias
  • Visual changes (blurring, yellow-green halo)
  • Headache, fatigue, drowsiness, confusion, seizures
41
Q

How can you reverse the toxicity of digoxin?

A

Digibind (antibody to digoxin)

42
Q

List the DDIs of digoxin?

A
  • Quinidine and Amiodarone increases plasma digoxin levels by decreasing elimination
  • Verapamil slow HR and digoxin toxicity
  • Diuretic can increase potential for arrhythmias due to hypokalemia
43
Q

Why does digoxin have so many DDIs?

A

it has a very narrow therapeutic window

44
Q

Long-term digoxin therapy may have what effect?

A

arrhythmias and worsened ventricular function

45
Q

What SYMPTOMS of CHF do diuretics treat?

A

promote Na+ and water excretion to reverse edema and pulmonary congestion

46
Q

Do diuretics really have an effect on CHF?

A

no, they just treat symptoms (reduce preload but do not increase CO)

47
Q

What 2 “high ceiling” diuretics are commonly used to treat CHF symptoms?

A

furosemide (“loop”)

Bumetanide

48
Q

What is typically used in combination with loop diuretics?

A

potassium sparing diuretics (like aldosterone antagonists)

49
Q

What is an example of an aldosterone antagonist?

A

spironolactone

50
Q

What are the adverse effects of diuretics?

A 
Electrolyte disturbances
Hypokalemia
Hyponatremia
Metabolic alkalosis 
Dehydration, hypotension
Ototoxicity (tinnitus and hearing loss from loop diuretics)
51
Q

What type of drugs reduce efficacy of diuretics by promoting fluid retention?

52
Q

What drugs mimic the effects of diuretics but have a suboptimal effect that is not sufficient enough to prevent edema?

A

ACE inhibitors and ARBs by reducing sodium retention by preventing aldosterone release)

53
Q

What effects does spironolactone and eplerenone (aldosterone inhibitors) have other than diuretic effect?

A

Stop the direct mitogenic and fibrogenic effects of aldosterone (combined with AngII) on the myocardium that often leads to worsened LV function

54
Q

What effect do direct arterial vasodilators have in CHF? Name an example used in CHF.

A

reduce afterload to improve ventricular performance and increase CO. Hydralazine

55
Q

What must you combine with a arterial vasodilator to reduce both afterload and preload?

A

a venodilator (nitrate)

56
Q

When would you give a patient hydralazine?

A

only if they are unable to tolerate ACE inhibitors (ex. renal insufficiency or angioedema)

57
Q

What are the adverse effects of hydralazine?

A

nausea
anorexia
+FANA
drug induced lupus (rare)

58
Q

How to nitrates reduce preload?

A

Veno and Vasodilation!!

  • Reduce pulmonary arterial pressure (pulmonary congestion)
  • Reduces left ventricular filling pressure and wall stress
  • these decrease preload and afterload
59
Q

Name the 2 IV inotropic agents.

A

dobutamine

milrinone

60
Q

What is the MOA of dobutamine.

A

Beta agonist and alpha agonist that vasodilates and serves as a “bridge” until the patient is stable enough for digoxin

61
Q

What drug should not be used with dobutamine?

A

beta-blocker therapy prevents the vasodilator effect of dobutamine and may actually cause vasoconstriction (from alpha 1 effect)

62
Q

What is a problem with dobutamine release?

A

desensitizaiton

63
Q

What drug works in the path of dobutamine but will not have the problem of desensitizaiton?

64
Q

What is the MOA of milrinone?

A

PDE inhibitor to stop the breakdown of cAMP. This will lead to increased HR and increase contraction speed!

65
Q

When are ANP and BNP released from the atria and ventricles?

A

in response to volume/pressure expansion

66
Q

What are the levels of ANP and BNP like in CHF? Why?

A

they are naturally elevated to promote vasodilation, venodilation, and natriuresis

67
Q

What are the hemodynamic effects of ANP and BNP?

A
  • Reduce preload
  • Inhibit renin/aldosterone release
  • Inhibits sodium reabsorption in proximal convoluted tubule
  • Selective afferent arteriolar vasodilation
68
Q

What is nesiritide? What is it approved for?

A

Nesiritide is recombinant human BNP approved for IV treatment of Class IV CHF

69
Q

What is the MOA of nesiritide?

A
  • Binds to BNP receptor in vascular smooth muscle, increases cGMP to promote veno-and vasodilation: this reduces preload and afterload
  • Increases GFR by dilating renal arterioles, natriuresis (decreases Na resorption)
  • Suppresses R-A-A and SNS
70
Q

Who should be given nesiritide?

A

Class IV CHF in patients who do not respond to nitroglycerin

71
Q

BE SURE TO LOOK AT CHART!

A

Don’t forget: BE SURE TO LOOK AT CHART!

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