Test 2 Pharm Flashcards by John Goodman

Furosemide

Class? mechanism of action? Clinical uses?

Diuretic

Inhibits Na+/K+/2Cl- cotransporter increasing [solute] which draws water into the lumen –> increased urine output

Edema, hypercalcemia, hypertension

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Furosemide toxicity?

hypokalemia, ototoxicity

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Lisonopril

Class? mechanism of action? Clinical uses?

RAAS drug

inhibits angiotensin converting enzyme (ACE)

CHF, hypertension, diabetic renal disease

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Lisonopril toxicity?

bradykinin cough reflex, hyperkalemia, teratogenic

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Valsartan

Class? mechanism of action? Clinical uses?

RAAS drug

angiotensin II receptor antagonist

CHF and hypertension

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Valsartan toxicity?

hyperkalemia, teratogenic

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spironolactone

Class? mechanism of action? Clinical uses?

RAAS drug

aldosterone receptor inhibitor

CHF, hypertension, hyperaldosteronism

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spironolactone toxicity?

hyperkalemia, endocrine effects

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Carvedilol

Class? mechanism of action? Clinical uses?

Beta blocker

B1 and alpha 1 antagonist

heart failure, hypertension

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Carvedilol toxicity?

bradycardia, bronchoconstriction, AV block, CNS sedation

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Metoprolol

Class? mechanism of action? Clinical uses?

Beta blocker/ class II antiarrhythmic

B1 antagonist

heart failure, hypertension, angina, arrhythmias

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Metoprolol toxicity?

bradycardia, AV block, CNS sedation

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Dobutamine

Class? mechanism of action? Clinical uses?

Inotrope and chronotrope

B1 agonist

heart failure

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Dobutamine toxicity?

arrhythmia

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digoxin

Class? mechanism of action? Clinical uses?

ionotrope/cardiac glycoside

inhibits Na+/K+ pump, which increases intracellular [Ca2+] via Na+/Ca2+ exchanger

heart failure, arrhythmias

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digoxin toxicity?

visual disturbances, nausea, arrhythmias

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Milrinone

Class? mechanism of action? Clinical uses?

inotrope

phosphodiesterase inhibitor which increases cAMP

heart failure

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Milrinone toxicity?

arrhythmia

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Hydralazine

Class? mechanism of action? Clinical uses?

Vasodilator

opens vascular K+ channels resulting in relaxation –> decreased afterload

heart failure, angina

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Hydralazine toxicity?

tachycardia, hypotension, headache

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Isosorbide dinitrate

Class? mechanism of action? Clinical uses?

vasodilator

nitric oxide mechanism

heart failure

Isosorbide dinitrate toxicity?

tachycardia, hypotension, headache

Sacubitril

Class? mechanism of action? Clinical uses?

Vasodilator

neprilysin inhibitor

heart failure

Sacubitril toxicity?

hyperkalemia, cough, hypotension

Procainamide Class? mechanism of action? Clinical uses?

Class IA antiarrhythmic inhibits Na+ channels (and K+ channels) supraventricular and ventricular arrhythmias, WPW syndrome

Lidocaine Class? mechanism of action? Clinical uses?

Class I antiarrhythmic inhibits Na+ channels (and K+ channels) ventricular tachycardia

Lidocaine Class? mechanism of action? Clinical uses?

Class IB antiarrhythmic inhibits Na+ channels (and K+ channels) ventricular tachycardia

Lidocaine toxicity?

CNS toxicity

Flecainide Class? mechanism of action? Clinical uses?

Class IC antiarrhythmic inhibits Na+ channels (and K+ channels) atrial tachycardia with normal ventricular function

Flecainide toxicity?

arrhythmia

What type of drugs are class II antiarrhythmics?

Beta blockers

Class I antiarrhythmic drugs block the _______ channels responsible for phase ___ of the cardiac action potential.

Class I drugs block sodium channels responsible for Phase 0 (upshoot) of the cardiac action potential

Amiodarone Class? mechanism of action? Clinical uses?

Class III antiarrhythmic Inhibits K+ and Na+ channels Atrial and ventricular tachycardias

Amiodarone toxicity

Long QT, hypotension, pulmonary fibrosis, tissue deposits, drug interactions

Dronaderone Class? mechanism of action? Clinical uses?

Class III antiarrhythmic Inhibits K+ and Na+ channels Atrial and ventricular tachycardias

Dronaderone toxicity?

long QT, depressed conduction

Dofetilide Class? mechanism of action? Clinical uses?

Class III antiarrhythmic Inhibits K+ Atrial and ventricular tachycardias

Dofetilide toxicity?

long QT

Sotalol Class? mechanism of action? Clinical uses?

Class III antiarrhythmic Inhibits K+ channels and Beta adrenergic receptors Atrial and ventricular tachycardias

Sotalol toxicity?

Long QT

Verapamil Class? mechanism of action? Clinical uses?

Class IV antiarrhythmic Voltage gated Ca2+ channel inhibitor, cardiac preferring (non-DHP) atrial arrhythmias, angina, hypertension

Verapamil toxicity

hypotension, tachycardia

Nifedipine Class? mechanism of action? Clinical uses?

L-type Ca2+ channel blocker (smooth muscle) Voltage gated Ca2+ channel inhibitor, vascular smooth muscle preferred (dilation) angina, hypertension

Nifedipine toxicity?

hypotension, tachycardia

Adenosine Class? mechanism of action? Clinical uses?

nucleotide receptor agonist activate adenosine receptors conversion of atrial arrhythmias

Adenosine toxicity?

Nadda! (well, none on our list)

What effect do class IC AADs have on the QRS complex? What about the effective refractory period?

Class IC AADs widen the QRS cuz they slow phase 0 (upstroke) a ton, but the ERP is unchanged.

What is the mechanism of action of class I AADs?

They block Na+ channels responsible for Phase 0 (upstroke) of the cardiac action potential

What is the mechanism of action of class III AADs? What effect do they have on the action potential and ERP?

They block K+ channels. Amiodarone and dronedarone inhibit Na+ channels, too. Action potential is prolonged, ERP is prolonged.

What is the mechanism of action of class IV AADs?

They block Ca2+ channels responsible for Phase 0 (upstroke) of the nodal pacemaker action potential for rate control.