2023-09-14T05:06:16+03:00[Europe/Moscow] en true <p>inhibits Na/K pump in cardiomycocytes to increase concentration of sodium &amp; calcium; slows the heart and increases the force of contraction </p>, <p>increases renal perfusion by decreasing renin production and increasing diuresis </p>, <p>increases CO; prevents neurohormonal activation by decreasing HR &amp; PR</p>, <p>increases parasympathetic outflow at SA and AV node; decreases AV node automaticity </p>, <p>f; affects sodium pumps of other excitable tissue</p>, <p>loop diuretics; these can cause hypokalemia &amp; hypomagnesemia </p>, <p>correct K/Mg deficiencies, anti-arrhythmic drugs, DigiFab </p>, <p>selectively inhibits cardiac pacemaker ion channels; causes hyperpolarization through funny (iF) channel; reduces heart rate</p>, <p>patients who are not receiving efficacy from BBs </p>, <p>dose</p>, <p>f; heart rate only</p>, <p>loop, thiazides, K+ sparing, SGLT2 inhibitors</p>, <p>vericiguat, BiDil </p>, <p>digoxin </p>, <p>ivabradine </p>, <p>a</p>, <p>b</p>, <p>c</p>, <p>a</p>, <p>loop; thiazide </p>, <p>Brain natriuretic Peptide (BNP</p>, <p>causes vasodilation of arterial &amp; venous blood vessels </p>, <p>causes potent natriuretic/diuretic effects</p>, <p>binds to natriuretic peptide receptors A; activates membrane-bound guanyly cylase; causes intracellular rise in cGMP</p>, <p>Nesiritide </p>, <p>preload; afterload; CO; ejection fraction </p>, <p>a,d </p>, <p>cardiac myocyte death</p>, <p>they increase energy expenditure &amp; have less time for coronary perfusion in diastole </p>, <p>a, b </p>, <p>c</p>, <p>c,d</p>, <p>a</p>, <p>predominate agonist activity towards B1; increases myocardial contractilty; increases CO </p>, <p>a,b,c</p>, <p>a,c</p>, <p>b</p>, <p>c</p>, <p>c</p>, <p>b</p>, <p>b</p>, <p>d</p>, <p>inhibits PDE3 to decrease cAMP degradation; activates PKA cascade to increase ca++ influx and increase contractility </p> flashcards
Digoxin, Ivabradine, Acute HF (Pharmacology)

Digoxin, Ivabradine, Acute HF (Pharmacology)

  • inhibits Na/K pump in cardiomycocytes to increase concentration of sodium & calcium; slows the heart and increases the force of contraction

    Digoxin MOA?

  • increases renal perfusion by decreasing renin production and increasing diuresis

    How does Digoxin affect the kidneys?

  • increases CO; prevents neurohormonal activation by decreasing HR & PR

    How does Digoxin affect the heart?

  • increases parasympathetic outflow at SA and AV node; decreases AV node automaticity

    How does Digoxin decrease heart rate?

  • f; affects sodium pumps of other excitable tissue

    Digoxin only affects cardiac muscle cells. T/F?

  • loop diuretics; these can cause hypokalemia & hypomagnesemia

    Which drugs can induce Digitalis toxicity? Why?

  • correct K/Mg deficiencies, anti-arrhythmic drugs, DigiFab

    How can we combat the AE's associated with Digoxin? (3)

  • selectively inhibits cardiac pacemaker ion channels; causes hyperpolarization through funny (iF) channel; reduces heart rate

    Ivabradine MOA?

  • patients who are not receiving efficacy from BBs

    Who do we use Ivabradine in?

  • dose

    Ivabradine provides a ________ dependent reduction of heart rate.

  • f; heart rate only

    Ivabradine reduces heart rate & contractility. T/F?

  • loop, thiazides, K+ sparing, SGLT2 inhibitors

    Which drugs are involves in preload reduction? (4)

  • vericiguat, BiDil

    Which drugs are involved in afterload reduction? (2)

  • digoxin

    Which drug is a positive inotropoic agent?

  • ivabradine

    Which drug is a heart rate reducer?

  • a

    Which is a VENODILATOR ?

    a) low dose nitroglycerin

    b) high dose nitroglycerin

    c) nitroprusside

  • b

    Which is an ARTERIAL VASODILATOR?

    a) low dose nitroglycerin

    b) high dose nitroglycerin

    c) nitroprusside

  • c

    Which is an EQUAL arterial & venous vasodilator?

    a) low dose nitroglycerin

    b) high dose nitroglycerin

    c) nitroprusside

  • a

    A patient comes in with Acute HF, they are presenting with dyspnea and showing signs of fluid overload/congestion? What should we treat them with?

    a) loop diuretic

    b) thiazide diuretic

    c) MRA diuretic

    d) hydralazine

  • loop; thiazide

    If a patient with Acute HF, is resistant to _______ diuretic we can add ______.

  • Brain natriuretic Peptide (BNP

    -secreted by the ventricles due to excessive myocardial stretch; part of

    HF compensatory mechanisms

  • causes vasodilation of arterial & venous blood vessels

    How does BNP affect the Vasculature?

  • causes potent natriuretic/diuretic effects

    How does BNP affect the kidneys?

  • binds to natriuretic peptide receptors A; activates membrane-bound guanyly cylase; causes intracellular rise in cGMP

    BNP MOA?

  • Nesiritide

    -synthetic analog of BNP for acute HF

  • preload; afterload; CO; ejection fraction

    Nesiritide decreases ____ & ____; while increasing _____ & _____.

  • a,d

    All positive inotropes increase the risk of _______.

    a) tachycardia

    b) bradycardia

    c) hypotension

    d) arrhythmias

  • cardiac myocyte death

    Positive inotropes can cause risk of _________, due to poor perfusion.

  • they increase energy expenditure & have less time for coronary perfusion in diastole

    Why can positive inotropes cause tachycardia?

  • a, b

    (+) enantiomer of Dobutamine agozines

    a) B1

    b) B2

    c) A1

    d) A2

  • c

    (-) enantiomer of Dobuatmine agonizes

    a) B1

    b) B2

    c) A1

    d) A2

  • c,d

    Agonizing B1 & B2 will cause

    a) vasoconstriction

    b) negative inotropism

    c) positive inotropism

    d) vasodilation

  • a

    Agonizing A1 will cause

    a) vasoconstriction

    b) negative inotropism

    c) positive inotropism

    d) vasodilation

  • predominate agonist activity towards B1; increases myocardial contractilty; increases CO

    Dobutamine MOA?

  • a,b,c

    Epinephrine is an agonist of

    a) B1

    b) B2

    c) A1

    d) A2

  • a,c

    Norepinephrine is an agonist of

    a) B1

    b) B2

    c) A1

    d) A2

  • b

    Which is a potent cardiac stimulant?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • c

    Which is a more potent vasoconstrictor?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • c

    Which causes TOO MUCH of an increase in afterload?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • b

    Which has positive inotropic & chronotropic actions?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • b

    Which has a 2-minute half-life?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • d

    Which is an inotropic agent and vasodilator (Inodilator)?

    a) dobutamine

    b) epinephrine

    c) norepinephrine

    d) milrinone

  • inhibits PDE3 to decrease cAMP degradation; activates PKA cascade to increase ca++ influx and increase contractility

    Milrinone MOA?