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Heart failure drugs

Total questions: 45

Worksheet time: 23mins

Name
Class
Date
1.

A patient at ⬆ risk for HF but without structural Heart disease or symptoms is in stage:

a)

A

b)

B

c)

C

d)

D

2.

A patient with structural Heart disease but without signs and symptoms is in stage:

a)

A

b)

B

c)

C

d)

D

3.

A patient with structural Heart disease but prior or current signs and symptoms is in stage:

a)

A

b)

B

c)

C

d)

D

4.

A patient with refractory HF requiring specialized interventions:

a)

A

b)

B

c)

C

d)

D

5.

LVEF < 40&%

a)

HFrEF

b)

HFmrEF

c)

HFpEF

6.

LVEF 40-49%

a)

HFrEF

b)

HFmrEF

c)

HFpEF

7.

LVEF > 50&

a)

HFrEF

b)

HFmrEF

c)

HFpEF

8.

Diuretics, MRA, digoxin are used to:

a)

Improve their clinical status

b)

Functional capacity

c)

Quality of life

d)

Prevent hospital admission

9.

Digoxin and blockers are used to:

a)

Improve their clinical status

b)

Functional capacity

c)

Quality of life

d)

Prevent hospital admission

10.

ACEIs, BB, hydralazine, and isosorbide dinitrate are used to:

a)

Improve their clinical status

b)

Functional capacity

c)

Quality of life

d)

Prevent hospital admission

11.

ARB, MRA, diuretics, sacubitril/valsartan, ivabradine, and digoxinare used to:

a)

Prevent hospital admission

b)

Quality of life

c)

Reduce mortality

d)

Improve their clinical status

12.

ACEIs, ARB, MRA, BB, sacubitril/valsartan, ivabradine are used to:

a)

Reduce mortality

b)

Prevent hospital admission

c)

Quality of life

d)

Improve their clinical status

13.

(Stage)

Goals:

1. Heart-healthy lifestyle

2. Prevent vascular, and coronary disease

3. Prevent LV structural abnormalities

Drugs: ACEI, ARBs, Statins

a)

A

b)

B

c)

C

d)

D

14.

(Stage)

Goals:

1. Prevent HF symtoms

3. Prevent further cardiac remodeling

Drugs: ACEI, ARBs, BB

a)

A

b)

B

c)

C

d)

D

15.

(Stage)

Goals:

1. Control symptoms

2. Improve HRQOL

3. Prevent hospitalization

4. Prevent mortality

Treatment: Diuresis, Revascularization or valvular surgery

a)

A

b)

C HFrEF

c)

C HFpEF

d)

D

16.

(Stage)

Goals:

1. Control symptoms

2. Patient education

3. Prevent hospitalization

4. Prevent mortality

Treatment: Diuresis, ACEIs, ARBs, BB, Aldosterone antagonist, Revascularization or valvular surgery, ICD, and CRT

a)

A

b)

C HFpEF

c)

C HFrEF

d)

D

17.

(Stage)

Goals:

1. Control symptoms

2. Improve HRQOL

3. Prevent hospitalization

4. Establush patient's end-of life goals

Treatment: heart transplant, chronic inotropes, MCS, surgery, Palliative care

a)

A

b)

B

c)

C

d)

D

18.

NYHA class II-IV

CrCl > 30 & K < 5

a)

Aldosterone antagonist

b)

Discontinue ACEI or ARB, Initiate ATreceptor neprilysin inhibitor

c)

Hydral-nitrates

d)

Cardioverter-defibrillator

19.

NYHA class II-III

Adequate BP on ACEI or ARB. No C/I to ARB or sacubritril

a)

Aldosterone antagonist

b)

Discontinue ACEI or ARB, Initiate ATreceptor neprilysin inhibitor

c)

ICD

d)

Hydral-nitrates

20.

NYHA class III-IV in black patients

a)

ICD

b)

Aldosterone antagonist

c)

Hydral-nitrates

d)

CRT

21.

NYHA class II-III LVEF < 35% >40 post MI

a)

Hydral-nitrates

b)

Aldosterone antagonist

c)

ICD

d)

CRT

22.

MAO: (-) SLC12A3 in the distal convoluted tubule -> (-) Na/H2O reabsorption in the nephron = vasodilation

a)

Hydrochlorothiazide

b)

Furosemide

c)

Spironolactone

d)

Mannitol

23.

MAO: competitive (-) NKCC2 in the thick ascending limb of the loop of Henle -> (-) H2O reabsorption, ⬆ excretion

a)

Furosemide

b)

Spironolactone

c)

Hydrochlorothiazide

d)

Mannitol

24.

Side effects: tinnitus, reversible or permanent hearing loss, or reversible deafness.

a)

Furosemide

b)

Hydrochlorothiazide

c)

Spironolactone

d)

Mannitol

25.

MAO: Competitive antagonist of aldosterone at the convoluted renal tubule -> ⬆ Na/water excretion, ⬆K retention.

Binds to mineralcorticoid receptor -> (-)Na+/K+-ATPase -> (-) Na+ K+ transport in the distal tubule.

a)

Spironolactone

b)

Mannitol

c)

Acetazolamide

d)

Furosemide

26.

It also has anti-androgenic activity. Progesterone agonist.

a)

Spironolactone

b)

Mannitol

c)

Acetazolamide

d)

Conivaptan

27.

⬆ the hypotensive activities of ACEI & ARB

a)

Spironolactone

b)

Furosemide

c)

Hydrochlorothiazide

d)

Mannitol

28.

Acute overdosage may be manifested by drowsiness, mental confusion, maculopapular or erythematous rash, nausea, vomiting, dizziness, or diarrhea. Also has been shown to be tumorigenic in chronic toxicity studies in rats.

a)

Spironolactone

b)

Mannitol

c)

Acetazolamide

d)

Conivaptan

29.

MAO: ⬆ plasma osmolality -> ⬆ shift of water from brain and tissues to interstitial fluid and plasma

a)

Mannitol

b)

Acetazolamide

c)

Conivaptan

d)

Digoxin

30.

Adverse effects: nephrotoxic.

a)

Mannitol

b)

Acetazolamide

c)

Conivaptan

d)

Digoxin

31.

MAO: (-) carbonic anhydrase -> ⬇ CO2 tension in the pulmonary alveoli -> ⬆ arterial O2.

⬇ availability of hydrogen ions for active transport in the renal tubule lumen.

a)

Conivaptan

b)

Acetazolamide

c)

Digoxin

d)

Sacubitril

32.

Toxicity: hepatoxicity, rash, fever, eosinophilia, and Steven Johnson Syndrome

a)

Acetazolamide

b)

Conivaptan

c)

Digoxin

d)

Sacubitril

33.

MAO: Antagonist of V1A/V2A -> ⬆ excretion of water (aquaresis)

a)

Conivaptan

b)

Digoxin

c)

Sacubitril

d)

Nesiritide

34.

MOA: (-) Na-K- ATPase membrane pump -> ⬆Na/Ca -> contractility

Also acts on the electrical activity of the heart, ⬆ the slope of phase 4 depolarization, ⬇ the AP duration, and ⬇ the maximal diastolic potential.

a)

Digoxin

b)

Sacubitril

c)

Nesiritide

d)

Conivaptan

35.

Toxicity includes ventricular tachycardia or ventricular fibrillation, or progressive bradyarrhythmias, or heart block, Blurred vision, yellow, green or blue chromatopsia (enhanced color intensity).

a)

Digoxin

b)

Sacubitril

c)

Nesiritide

d)

Conivaptan

36.

Beta blockers: May increase the bradycardic activities of this drug.

a)

Sacubitril

b)

Digoxin

c)

Nesiritide

d)

Acetazolamide

37.

MAO: Active form LBQ657 -> (-) neprilysin -> ⬇ breakdown and ⬆ NP, ⬆ vasocontrictio by ⬆ AT2.

+ Vasaltan = (-) AT2 -> ⬇ resistance and BP

a)

Sacubitril

b)

Digoxin

c)

Nesiritide

d)

Digoxin

38.

MAO: Recombinant form of BNP -> ⬆ cGMP -> Smooth muscle relaxation.

a)

Nesiritide

b)

Sacubitril

c)

Digoxin

d)

Conivaptan

39.

Prazosin, terazosin and Doxazosin acts in vasculature by ⬇ vasoconstriction.

a)

a-1 blockers

b)

a-2 agonist

c)

ACEis

d)

ARBs

40.

Clonidine stimulate CNS alpha receptors -> vasodilation

a)

a-1 blockers

b)

a-2 agonist

c)

ACEis

d)

ARBs

41.

Lisonopril, Captopril and Enalapril, (-) AT1 to At2 conversion -> ⬇ vasoconstriction and ⬇fluid retention.

a)

a-1 blockers

b)

a-2 agonist

c)

ACEis

d)

ARBs

42.

Losartan, Valsartan and Candesartan Binds to AT2R-> block AT2 -> ⬇ vasoconstriction and ⬇ fluid retention.

a)

ACEis

b)

ARBs

c)

CCB

d)

Diuretics

43.

Propranolol, Metoprolol and Nebivolol in the heart -> ⬇ contractility, ⬇ HR and ⬇ CO.

In the CNS -> block sympathetic

a)

ARBs

b)

BB

c)

CBB

d)

ACEis

44.

Amlodipine, Nifedipine, Nicardine block Ca influx -> vasodilation

a)

DD CCB

b)

ND CCB

45.

Verapamil and Diltiazem vasodilation in sm and block Ca in myocytes and SA cells -> vasodilation, ⬇ HR and ⬇ contractility.

a)

DD CCB

b)

ND CCB