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Pharm II > Final New Material > Flashcards

Final New Material Flashcards

1
Q

AHA/ACC: Patients at high risk for HF but without structural heart disease or symptoms of HF

A

Stage A

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2
Q

AHA/ACC: Patients with structural heart disease but without signs/symptoms of HF

A

Stage B

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3
Q

AHA/ACC: Patients with structural heart disease with prior or current symptoms of HF

A

Stage C

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4
Q

AHA/ACC: Patients w/ refractory HF requiring specialized interventions

A

Stage D

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5
Q

NYHA: No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (SOB)

A

Class I - Mild

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6
Q

NYHA: Slight limitation of physical activity; comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea

A

Class II - Mild

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7
Q

NYHA: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea

A

Class III - Moderate

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8
Q

NYHA: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased

A

Class IV - Severe

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9
Q

Drugs for routine use in HFrEF pts (according to AHA/ACC algorithm)

A

Diuretics, ACEI or ARB, Beta Blocker, Aldosterone antagonists

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10
Q

Patients on the far right side of the Frank-starling curve have

A

congestive symptoms

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11
Q

Patients on the bottom portion of the Frank-starling curve have

A

low CO symptoms

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12
Q

X & Y axis of Frank-starling graph

A

X: End Diastolic Volume (Preload)
Y: Stroke Volume

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13
Q

Beta blockers commonly chosen as first-line for HF

A

Metoprolol, Carvedilol, Bisoprolol

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14
Q

2 drugs that make up Entresto

A

Valsartan (ARB) + Sacubitril (Neprilysin inhibitor)

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15
Q

Entresto is approved for:

A

Stage II-IV HF patients in place of an ACEI or ARB

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16
Q

Side Effects of Entresto

A

Hypotension, angioedema

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17
Q

Entresto is CONTRAINDICATED in

A

Pregnancy, pts w/ Renal Artery Stenosis

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18
Q

Medications to avoid while taking Entresto

A

another ARB or ACEI (or within 36hrs of previous ACEI use)

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19
Q

MOA of Ivabradine

A

Funny channel inhibitor (If); reduces activity of SA node - reducing HR

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20
Q

Ivabradine is indicated for pts w/

A

resting HR 70bpm or higher that are on maximally tolerated dose of Beta Blocker

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21
Q

Target HR for patients w/ heart failure

A

50-60bpm

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22
Q

Avoid taking Ivabradine in pts w/

A
  1. Sick sinus syndrome or conduction problems
  2. Dependent on pacemaker
  3. Pregnant or breastfeeding
  4. Dose-adjust or avoid in combo w/ CYP3A4 inhibitors
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23
Q

Side Effects of Ivabradine

A

Bradycardia, Hypertension, Phosphenes

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24
Q

In patients on optimized background therapy complaining of DYSPNEA, add on

A

Venous dilator - Isosorbide Dinitrate

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25
Q

In patients on optimized background therapy complaining of FATIGUE, add on

A

Arteriole dilator - Hydralazine

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26
Q

In Black patients on optimized background therapy complaining of symptoms, add on

A

BiDil (hydralazine/isosorbide dinitrate)

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27
Q

MC inotropic agent used for outpatient treatment

A

Digoxin

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28
Q

Inotropes available for in-patient treatment

A

PDE inhibitors & adrenergic receptor agonists

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29
Q

MOA of Digoxin

A

Na/K ATPase inhibitor

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30
Q

Effects of digoxin

A

Positive inotrope; decreases HR and increases PR interval

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31
Q

Side effects of digoxin

A

GI (anorexia, N, V, D)
Yellow/green halos; change in color perception
Dysrhythmia (increased w/ hypokalemia & hypercalcemia)

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32
Q

Indications of Digoxin toxicity

A

Ingested more than 6mg of Digoxin
Serum digoxin > 6ng/mL
Serum potassium > 6mEG/L

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33
Q

Treatments for Digoxin toxicity

A

DigiFab or Digibind

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34
Q

Inotropes besides Digoxin

A

Inamrinone, Milrinone, Dobutamine, Dopamine

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35
Q

MOA of Inamrinone & Milrinone

A

PDE-3 inhibitors; increase cAMP in cardiomyocytes

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36
Q

Side Effects of Inamrinone & Milrinone

A

Hepatoxicity, myelosuppressive, increased risk of dysrhythmia

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37
Q

Which is less hepatotoxic & myelosuppressive? Inamrinone or Milrinone

A

Milrinone

38
Q

MOA of dobutamine

A

Beta 1 selective agonist

39
Q

Effects of dopamine at moderate dose

A

improves cardiac contractility

40
Q

Effects of dopamine at high doses

A

Improves cardiac contractility but also increases BP

41
Q

Synthetic BDNF/BNP
Causes natriuresis, vasodilation, reduces RAAS
Does not improve mortality or re-hospitalization rates

A

Nesiritide (Natrecor)

42
Q

Endothelin receptor antagonist
Only used in pts w/ right-sided HF secondary to pulmonary HTN

A

Bosentan (Tracleer)

43
Q

ADH receptor antagonist for hyponatremia in HF

A

Conivaptan (Vaprisol)

44
Q

Class I Antidysrhythmic MOA

A

Na channel blockers

45
Q

Class II Antidysrhythmic MOA

A

beta-blockers

46
Q

Class III Antidysrhythmic MOA

A

Prolong APD usually due to K-channel blockade

47
Q

Class IV Antidysrhythmic MOA

A

Calcium Channel Blockers

48
Q

Na channel blocker; Prolongs APD –> risk of Torsades

A

Class IA Antidysrhythmics: Disopyramide; Quinidine; Procainamide

49
Q

Class and SE of Quinidine

A

Class IA antidysrhythmic; Cinchonism (dizziness, HA, tinnitus)

50
Q

Class and SE of Procainamide

A

Class IA antidysrhythmic; anti-histone antibody lupus

51
Q

Class and SE of Disopyramide

A

Class IA antidysrhythmic; antimuscarinic effects

52
Q

Na channel blocker; Shortens APD; preferentially binds to ischemic tissue

A

Class IB Antidysrhythmics; Lidocaine & Mexiletine

53
Q

Na channel blocker; doesn’t change APD

A

Flecainide & Propafenone

54
Q

SE of Class IC antidysrhythmics

A

increased mortality when used in patients with structural cardiac defects

55
Q

Class and SE of Flecainide

A

Class IC antidysrhythmic; binds to pulmonary tissue; a/w interstitial lung dz

56
Q

Less effective than class I antidysrhythmics but better tolerated long term; useful for tachy-dysrhythmias (prolong RR interval and PR interval)

A

Class II - Beta-blockers; Metoprolol, atenolol, propranolol
Esmolol (if emergent)
Sotalol - also has class III activity

57
Q

Class III Anti-dysrhythmics

A

Sotalol
Dofetilide
Ibutilide
Bretylium
Amiodarone
Dronedarone

58
Q

Which class III antidysrhythmics are MOST a/w torsades

A

Dofetilide & Ibutilide

59
Q

MOA of Bretylium

A

class III antidysrhythmic; blocks K channels and inhibits release of NE from sympathetic terminals

60
Q

SE of Amiodarone

A

may affect thyroid function; photodermatitis; vision changes; hepatotoxicity; pulmonary fibrosis

61
Q

SE of Dronedarone

A

CONTRAINDICATED in pregnancy; rare cases of pulmonary disease; still need to monitor liver function

62
Q

Class IV Antidysrhythmics

A

Verapamil & Diltiazem

63
Q

Effect of Class IV antidysrhythmics

A

Reduce conduction and increase refractory period

64
Q

SE of class IV

A

do NOT use in patients with WPW syndrome

65
Q

DOC for rapid conversion of SVT

A

Adenosine

66
Q

MOA of Adenosine

A

A1R activation causes K-induced hyperpolarization of AV node

67
Q

Use of Digoxin

A

atrial dysrhythmias - particularly secondary to HF

68
Q

Digoxin is contraindicated in

A

pts w/ WPW

69
Q

Uses of Magnesium

A

Digoxin & quinidine-induced dysrhythmias
Torsades

70
Q

SE of magnesium

A

may cause flushing and hypotension secondary to smooth muscle relaxation

71
Q

MOA of statins

A

HMG-CoA reductase inhibitors

72
Q

Low potency statins

A

Lovastatin, Pravastatin, Fluvastatin

73
Q

Moderate Potency statins

A

Simvastatin, Pitavastatin

74
Q

High potency statins

A

Atorvastatin, Rosuvastatin

75
Q

SE of Statins

A

increased liver enzymes, rhabdomyolysis, CYP450 inhibitors (except pitavastatin)
CONTRAINDICATED in pregnancy & in children

76
Q

SE of Niacin

A

Flushing (prostaglandin induced), GI intolerance - avoid in pts w/ active peptic ulcer dz, increased liver enzymes, plasma glucose, uric acid

77
Q

Fibrates

A

Fenofibrate & Gemfibrozil

78
Q

MOA of Fibrates

A

PPAR-alpha ligands

79
Q

Use of fibrates

A

Decreases release of triglycerides into plasma and increases tissue utilization of triglycerides; long-term therapy will usually also decrease cholesterol

80
Q

SE of Fibrates

A

cholesterol gall stones, increased liver enzymes, potentiate anticoagulant effects (esp warfarin)

81
Q

Use of Omega 3 fatty acids

A

lower triglycerides in combo w/ diet & exercise

82
Q

Very potent reduction of triglycerides; cholesterol often increases by same amount

A

Omega-3-acid ethyl ester (EPA/DHA combination)

83
Q

Less potent reduction of triglycerides; does not increase cholesterol

A

Icosapent ethyl (pure EPA)

84
Q

SE of Omega-3 fatty acids

A

anticoagulants may be potentiated; increased risk of A-fib and # of A-fib episodes

85
Q

Bile Acid Binding Resins

A

Cholestyramine, Colestipol, Colesevelam

86
Q

SE of Bile acid binding Resins

A

Binds to other drugs - avoid co-admin; Constipation; triglycerides may increase as cholesterol decreases

87
Q

MOA of Ezetimibe

A

Neimann-Pick C1-Like 1 transporter inhibitor; inhibits absorption of food-derived cholesterol

88
Q

4 groups to start statin therapy

A
  1. LDL > 190
  2. Diabetics
  3. Pts w/ clinically significant atherosclerotic disease
  4. ASCVD risk > 7.5%
89
Q

PCSK9 Inhibitors

A

Evolucumab & Alirocumab

90
Q

MOA of Ranolazine

A

alters Na-dependent Ca channel conductance during ischemia; reduces calcium overloading during ischemia; reduces contractility (reduces O2 requirement)
Inhibits fatty-acid oxidation in cardiomyocytes; reduces oxygen requirement per ATP produced

91
Q

SE of Ranolazine

A

avoid in pts w/ liver failure; dose adjust when used w/ strong p450 inhibitors and CYP2D6 substrates (ranolazine inhibits CYP2D6)

Pharm II (5 decks)

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