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

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

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

A

Stage B

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

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

A

Stage C

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

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

A

Stage D

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

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

A

Class I - Mild

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

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

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

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

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

A

Diuretics, ACEI or ARB, Beta Blocker, Aldosterone antagonists

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

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

A

congestive symptoms

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

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

A

low CO symptoms

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

X & Y axis of Frank-starling graph

A

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

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

Beta blockers commonly chosen as first-line for HF

A

Metoprolol, Carvedilol, Bisoprolol

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

2 drugs that make up Entresto

A

Valsartan (ARB) + Sacubitril (Neprilysin inhibitor)

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

Entresto is approved for:

A

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

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

Side Effects of Entresto

A

Hypotension, angioedema

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

Entresto is CONTRAINDICATED in

A

Pregnancy, pts w/ Renal Artery Stenosis

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

Medications to avoid while taking Entresto

A

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

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

MOA of Ivabradine

A

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

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

Ivabradine is indicated for pts w/

A

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

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

Target HR for patients w/ heart failure

A

50-60bpm

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

Side Effects of Ivabradine

A

Bradycardia, Hypertension, Phosphenes

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

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

A

Venous dilator - Isosorbide Dinitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
In patients on optimized background therapy complaining of FATIGUE, add on
Arteriole dilator - Hydralazine
26
In Black patients on optimized background therapy complaining of symptoms, add on
BiDil (hydralazine/isosorbide dinitrate)
27
MC inotropic agent used for outpatient treatment
Digoxin
28
Inotropes available for in-patient treatment
PDE inhibitors & adrenergic receptor agonists
29
MOA of Digoxin
Na/K ATPase inhibitor
30
Effects of digoxin
Positive inotrope; decreases HR and increases PR interval
31
Side effects of digoxin
GI (anorexia, N, V, D) Yellow/green halos; change in color perception Dysrhythmia (increased w/ hypokalemia & hypercalcemia)
32
Indications of Digoxin toxicity
Ingested more than 6mg of Digoxin Serum digoxin > 6ng/mL Serum potassium > 6mEG/L
33
Treatments for Digoxin toxicity
DigiFab or Digibind
34
Inotropes besides Digoxin
Inamrinone, Milrinone, Dobutamine, Dopamine
35
MOA of Inamrinone & Milrinone
PDE-3 inhibitors; increase cAMP in cardiomyocytes
36
Side Effects of Inamrinone & Milrinone
Hepatoxicity, myelosuppressive, increased risk of dysrhythmia
37
Which is less hepatotoxic & myelosuppressive? Inamrinone or Milrinone
Milrinone
38
MOA of dobutamine
Beta 1 selective agonist
39
Effects of dopamine at moderate dose
improves cardiac contractility
40
Effects of dopamine at high doses
Improves cardiac contractility but also increases BP
41
Synthetic BDNF/BNP Causes natriuresis, vasodilation, reduces RAAS Does not improve mortality or re-hospitalization rates
Nesiritide (Natrecor)
42
Endothelin receptor antagonist Only used in pts w/ right-sided HF secondary to pulmonary HTN
Bosentan (Tracleer)
43
ADH receptor antagonist for hyponatremia in HF
Conivaptan (Vaprisol)
44
Class I Antidysrhythmic MOA
Na channel blockers
45
Class II Antidysrhythmic MOA
beta-blockers
46
Class III Antidysrhythmic MOA
Prolong APD usually due to K-channel blockade
47
Class IV Antidysrhythmic MOA
Calcium Channel Blockers
48
Na channel blocker; Prolongs APD --> risk of Torsades
Class IA Antidysrhythmics: Disopyramide; Quinidine; Procainamide
49
Class and SE of Quinidine
Class IA antidysrhythmic; Cinchonism (dizziness, HA, tinnitus)
50
Class and SE of Procainamide
Class IA antidysrhythmic; anti-histone antibody lupus
51
Class and SE of Disopyramide
Class IA antidysrhythmic; antimuscarinic effects
52
Na channel blocker; Shortens APD; preferentially binds to ischemic tissue
Class IB Antidysrhythmics; Lidocaine & Mexiletine
53
Na channel blocker; doesn't change APD
Flecainide & Propafenone
54
SE of Class IC antidysrhythmics
increased mortality when used in patients with structural cardiac defects
55
Class and SE of Flecainide
Class IC antidysrhythmic; binds to pulmonary tissue; a/w interstitial lung dz
56
Less effective than class I antidysrhythmics but better tolerated long term; useful for tachy-dysrhythmias (prolong RR interval and PR interval)
Class II - Beta-blockers; Metoprolol, atenolol, propranolol Esmolol (if emergent) Sotalol - also has class III activity
57
Class III Anti-dysrhythmics
Sotalol Dofetilide Ibutilide Bretylium Amiodarone Dronedarone
58
Which class III antidysrhythmics are MOST a/w torsades
Dofetilide & Ibutilide
59
MOA of Bretylium
class III antidysrhythmic; blocks K channels and inhibits release of NE from sympathetic terminals
60
SE of Amiodarone
may affect thyroid function; photodermatitis; vision changes; hepatotoxicity; pulmonary fibrosis
61
SE of Dronedarone
CONTRAINDICATED in pregnancy; rare cases of pulmonary disease; still need to monitor liver function
62
Class IV Antidysrhythmics
Verapamil & Diltiazem
63
Effect of Class IV antidysrhythmics
Reduce conduction and increase refractory period
64
SE of class IV
do NOT use in patients with WPW syndrome
65
DOC for rapid conversion of SVT
Adenosine
66
MOA of Adenosine
A1R activation causes K-induced hyperpolarization of AV node
67
Use of Digoxin
atrial dysrhythmias - particularly secondary to HF
68
Digoxin is contraindicated in
pts w/ WPW
69
Uses of Magnesium
Digoxin & quinidine-induced dysrhythmias Torsades
70
SE of magnesium
may cause flushing and hypotension secondary to smooth muscle relaxation
71
MOA of statins
HMG-CoA reductase inhibitors
72
Low potency statins
Lovastatin, Pravastatin, Fluvastatin
73
Moderate Potency statins
Simvastatin, Pitavastatin
74
High potency statins
Atorvastatin, Rosuvastatin
75
SE of Statins
increased liver enzymes, rhabdomyolysis, CYP450 inhibitors (except pitavastatin) CONTRAINDICATED in pregnancy & in children
76
SE of Niacin
Flushing (prostaglandin induced), GI intolerance - avoid in pts w/ active peptic ulcer dz, increased liver enzymes, plasma glucose, uric acid
77
Fibrates
Fenofibrate & Gemfibrozil
78
MOA of Fibrates
PPAR-alpha ligands
79
Use of fibrates
Decreases release of triglycerides into plasma and increases tissue utilization of triglycerides; long-term therapy will usually also decrease cholesterol
80
SE of Fibrates
cholesterol gall stones, increased liver enzymes, potentiate anticoagulant effects (esp warfarin)
81
Use of Omega 3 fatty acids
lower triglycerides in combo w/ diet & exercise
82
Very potent reduction of triglycerides; cholesterol often increases by same amount
Omega-3-acid ethyl ester (EPA/DHA combination)
83
Less potent reduction of triglycerides; does not increase cholesterol
Icosapent ethyl (pure EPA)
84
SE of Omega-3 fatty acids
anticoagulants may be potentiated; increased risk of A-fib and # of A-fib episodes
85
Bile Acid Binding Resins
Cholestyramine, Colestipol, Colesevelam
86
SE of Bile acid binding Resins
Binds to other drugs - avoid co-admin; Constipation; triglycerides may increase as cholesterol decreases
87
MOA of Ezetimibe
Neimann-Pick C1-Like 1 transporter inhibitor; inhibits absorption of food-derived cholesterol
88
4 groups to start statin therapy
1. LDL > 190 2. Diabetics 3. Pts w/ clinically significant atherosclerotic disease 4. ASCVD risk > 7.5%
89
PCSK9 Inhibitors
Evolucumab & Alirocumab
90
MOA of Ranolazine
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
SE of Ranolazine
avoid in pts w/ liver failure; dose adjust when used w/ strong p450 inhibitors and CYP2D6 substrates (ranolazine inhibits CYP2D6)