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175 Cards in this Set
- Front
- Back
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Only diuretic to show reduced mortality in treatment of heart failure
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Spironolactone
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Competitive inhibitor of aldosterone receptor
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Spironolactone
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Diuretic which may induce hyperkalemia at the expense of preventing hypokalemia
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Spironolactone
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Active metabolite, canrenone, has half life of 16 hours
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Spironolactone
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May alter digitalis clearance
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Spironolactone
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May cause gynecomastia and menstrual irregularities due to blockage of other steroid receptors
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Spironolactone
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Diuretic with contraindication of hyperkalemia
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Spironolactone
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Diuretic which blocks Na/K/Cl channels in thick ascending limb
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Furosemide (Lasix)
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Diuretic which blocks Na/Cl symport in distal convoluted tubule. Also modified by ADH.
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Hydrochlorothiazide
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Indicated for acutely decompensated heart failure associated with HTN
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Nitroprusside
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Acts by releasing NO, which in turn lowers cardiac afterload and increases CO
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Nitroprusside
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Reduced to thiocyanate in the liver, prolonged doses may lead to toxicity
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Cyanide, as released with NO with dose of nitroprusside
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Peak time of nitroprusside action
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2 minutes
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Nitroprusside contraindication
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Hypotension
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Relaxes both arterioles and venules, with greater effect on arterioles
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Nitroprusside
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Vasodilator commonly used with isorbide dinitrate
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Hydralazine
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Vasodilator of unknown mechanism which causes predominately arterial and less venule dilation.
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Hydralazine
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Results in reflex tachycardia with increased renin and fluid retention
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Hydralazine
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May cause drug-induced lupus (10%)
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Hydralazine
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Denitrated through a variety of mechanisms to produce NO
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Nitroglycerin
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Potent vasodilator, diuretic, and natriuretic peptide released from kininogen via kallikrein
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Bradykinin
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Common side effect of enalapril
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Cough (20%) due to polymorphic BK-2 receptor causing bronchospasm
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Inactivates bradykinin
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ACE
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Enalapril
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ACE inhibitor (also spares bradykinin effects)
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May cause angioedema (0.5%)
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Enalapril
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Common enalapril side effects
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hypotension
hyperkalemia impaired renal function |
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Use in heart failure patients who cannot tolerate effects of ACEIs (cough/angioedema)
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ATN receptor blockers (ARBs)
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Blocks AT-1 receptors, producing vasodilation (without bradykinin effect)
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Losartan
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Initially, may cause a decrease in left ventricular systolic function, with an increase beyond baseline in 2-6 months
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Beta-blockers
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Beta-blocker with huge first-pass metabolism
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Metoprolol
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Side effects include bradycardia, hypotension, impaired response to hypoglycemia, and bronchospasm.
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Beta-blockers
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Carvedilol
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Non-selective beta and alpha-1 blocker
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Metoprolol
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Selective beta-1 blocker
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Propranolol
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Non-selective beta blocker
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Used for acute decompensated heart failure, with increased mortality used long-term
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Beta-agonists
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Stimulates beta-1 and beta-2 receptors
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Dobutamine
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At low doses, causes vasodilation. At high doses, causes vasoconstriction. Intermediate dose yield beta-agonist effect.
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Dobutamine
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Reserved inotrope for hypotensive patients.
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Dobutamine
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Inhibits breakdown of cAMP by phosphodiesterase 3
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Milrinone
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Contraindicated in ischemic heart disease
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Dobutamine
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Bypiridine which increases contractility and peripheral dilation
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Milrinone
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Causes thrombocytopenia (10%)
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Milrinone
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Bypiridine similar to milrinone, but not used secondary to higher incidence of thrombocytopenia
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Inamrinone
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Inhibits Na/K ATPase resulting in increased intracellular Ca++
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Digoxin
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May cause AV block, a-tach, v-fib, and bradycardia
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Digoxin
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Less is more when it comes to dosing
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Digoxin
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Spironolactone's interaction with digoxin
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Spironolactone decreases digoxin clearance
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Broad-spectrum antibiotics' interaction with digoxin
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Increases plasma digoxin levels
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Most common drugs that increase plasma digoxin levels
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Quinidine
Amiodarone |
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Digoxin antibody given in severe toxicity
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Digibind
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Captopril
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ACEI
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Eplerenone
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Aldosterone receptor blocker
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Synthetic BNP resulting in cGMP production
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Nesiritide
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Prodrugs which act as NO sources
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Organic nitrates
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Peak concentration time of organic nitrates
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4 minutes
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Organic nitrate metabolized extensively by first-pass mechanism.
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Isorbide dinitrate
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Most common side effect of organic nitrates
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Headache
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Preferentially dilates veins over arteries
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Organic nitrates
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Organic nitrates' contraindication
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Use with "viagra-type" drugs
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Every patient following an infarction should be on one of these agents
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Beta-blockers
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The use of this particular Ca-channel blocker increases mortality when given post MI
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Nifedipine
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Ca++ channel blocker mechanism
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Bind to alpha 1 subunit of L-type Ca++ channels
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Nifedipine class
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Dihydropyridine
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Diltiazem class
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Benzothiazepine
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Verapamil class
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Phenylalkylamine
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Ca++ channel blocker that is a potent vasodilator with little effect on contractility/automaticity
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Nifedipine
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Ca++ channel blocker that is a potent suppressor of automaticity, moderate vasodilator, and mild suppressor of contractility
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Diltiazem
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Ca++ channel blocker that is a potent suppressor of automaticity and contractility
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Verapamil
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Verapamil and diltiazem side effects
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Hypotension
Bradycardia |
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Diltiazem and nifedipine side effects
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Hypotension with reflex tachycardia
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Indicated in chronic stable angina, refractory to beta-blockers, Ca++ channel blockers, and organic nitrates
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Ranolazine
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Causes prolonged QT syndrome
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Ranolazine
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Disrupts Ranolazine metabolism, leading to toxicity
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Hepatic CYP3A4 system
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Inhibits hepatic CYP3A4 system, leading to Ranolazine toxicity
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Diltiazem
Verapamil Grapefruit Macrolide antibiotics HIV protease inhibitors |
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Used in the prevention of MI and in acute treatment of unstable angina
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Anti-platelet drugs
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Inhibits cycloxygenase, preventing formation of PGG2, PGH2, and Thromboxane A2 (via thromboxane synthetase)
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Acetylsalicylic Acid (ASA)
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Ticagrelor class
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Thienopyridine
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Ticlopidine class
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Thienopyridine
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Clopidogrel class
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Thienopyridine
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Inhibits ADP-mediated platelet activation via P2Y12-receptor blockade
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Ticagrelor
Ticlopidine (Ticlid) Clopidogrel (Plavix) |
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Inhibits glycoprotein IIb/IIIa aggregation in response to ADP-binding P2Y12 receptor. (IIb/IIIa aggregation allows fibrinogen to bind)
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Abciximab
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Fab fragment of a humanized monoclonal antibody
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Abciximab
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ASA half-life and effect
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short half-life, permanent COX inhibition (life of platelet 7-10 days)
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Ticlopidine half-life and effect
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short half-life, permanent P2Y12 inhibition (life of platelet 7-10 days)
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Clopidogrel half-life and effect
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Prodrug with longer half-life and slow onset of action
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Anti-platelet drug which may cause thrombocytopenia
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Abciximab
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Anti-platelet drug which may cause neutropenia (2%)
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Ticlopidine
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Indicated for treatment of anemia associated with chronic kidney disease, surgery, AIDS, or chemotherapy.
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Epoetin alpha
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Epoetin alpha half-life
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4-8 hours, yet effect is sufficient to warrant dose 3x/week
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May cause migratory thrombophlebitis, PE, or thrombosis
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Epoetin alpha
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May result in functional iron-deficiency
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Epoetin alpha
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Granulocyte-macrophage colony-stimulating factor
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Sargramostim
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Indicated prior to autologous bone marrow transplant
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Sargramostim
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Indicated after autologous bone marrow transplant
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Filgrastim
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Granulocyte colony-stimulating factor
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Filgrastim
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Indicated in iron-deficient anemia
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Ferrous sulfate
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Results from high iron intake with in patients genetically predisposed
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Hemochromatosis
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Amount of time needed to determine effectiveness of ferrous sulfate dose
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3-4 weeks
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What is cyanocobalamin?
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Vitamin B12
duh |
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May be given in hemolytic anemia
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Folic acid
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May counteract the antiepileptic effect of phenobarbitol, phenytoin, and primidone in large doses
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Folic acid
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Indicated treatment for DVT/PE and acute MI
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Heparin
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Antithrombin III (ATIII)
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Reacts irreversibly with activated serine proteases and neutralizes them
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Binds lysine residue on ATIII, multiplying its effect 100 fold
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Heparin
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Heparin clearance method
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Cleared and degraded by the reticuloendothelial system
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May result in osteoporosis and hyperkalemia (from inhibition of aldosterone)
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Heparin
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Anticoagulant that results in thrombocytopenia (0.5%)
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Heparin
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LMWH with primary activity against factor Xa
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Enoxaparin (Lovenox)
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Synthetic pentasaccharide that is a factor Xa inhibitor
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Fondaparinux
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LMWH / Fondaparinux contraindications
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Renal failure
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Isolated from salmon sperm
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Protamine sulfate
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Heparin inhibitor at low dose (high dose anti-coagulates)
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Protamine sulfate
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Synthetic derivative of hirudin, found in the salivary glands of a leech
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Lepirudin
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Synthetic direct thrombin inhibitor
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Lepirudin
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Indicated treatment in patients with heparin-induced thrombocytopenia
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Lepirudin
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Indicated as an alternative to lepirudin
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Argatroban
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Synthetic compound based on the structure of L-arginine and reversibly inhibits thrombin
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Argotroban
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Effective in preventing clots in patients with prosthetic heart valves or chronic a-fib
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Warfarin
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Vitamin K antagonist
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Warfarin
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Therapeutic doses decrease vitamin K-dependent coagulation factor production by 50%
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Warfarin
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Warfarin effective time
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3-5 days
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Warfarin dosage
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2-10 mg per day
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May cause birth defects
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Warfarin
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Causes purple toe syndrome
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Warfarin
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May cause skin necrosis
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Warfarin
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Monitors warfarin therapy
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PT
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Monitors heparin therapy
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PTT
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Indicated as an alternative to warfarin and are oral thrombin inhibitors
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Dabigatran (Pradaxa)
Rivaroxaban |
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Absorbed as inactive ester, which is hydrolyzed forming active drug
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Dabigatran
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Thrombin inhibitor with 5% bioavailability
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Dabigatran
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May be used in patients with nonvalvular a-fib
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Dabigatran
Rivaroxaban |
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Produced by beta-hemolytic streptococci
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Streptokinase
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Binds and activates plasminogen (lyses fibrin)
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Streptokinase
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Recombinant forms of t-PA
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Alteplase
Reteplase |
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Indicated in dissolving acute clots
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Fibrinolytic drugs
(alteplase, reteplase, streptokinase) |
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May result in ICH (1%)
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Fibrinolytic drugs
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Used to reduce bleeding post op in hemophiliacs
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Aminocaproic Acid
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Competes for lysine binding sites on plasminogen and plasmin, inhibiting interaction with fibrin
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Aminocaproic Acid
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May cause excessive thrombosis
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Aminocaproic Acid
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Inhibits adenosine-mediated platelet aggregation, while increasing cGMP and dilating coronary arteries
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Dipyridamole
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Cilostazol
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Reduces platelet aggregation
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Phytonoadone
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Vitamin K
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Peginesatide
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Erythropoiesis-stimulating agent
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Romiplostim
Eltrombopag |
Thrombopoiesis-stimulating agents
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Use in sickle cell disease
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Hydroxyurea
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Pyridoxine
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B6
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Thiamine
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B1
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State-dependent blocking
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With each AP, drugs bind and block Na+ channels. With each diastolic interval, drugs dissociated and "unblock" channels
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Class I Antiarrhythmics
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block Na+ channels, increasing threshold potential and decreasing Vmax of depolarization
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Class II Antiarrhythmics
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block sympathetic actions on the heart
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Class III antiarrhythmics
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Prolongs AP via K+ and Na+ channel blockade
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Class IV antiarrhythmics
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Ca++ channel blockade
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Class I antiarrhythmic which lowers resting membrane potential through preferentially blocking Na+ channels
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Quinidine
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Can be used in combination with digoxin in treatment of a-fib
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Quinidine
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May cause cinchonism
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Quinidine
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Similar to quinidine, these drugs treat supraventricular and ventricular arrhythmias
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Procainamide
Disopyramide |
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Hyperkalemia may predispose drug toxicity
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Procainamide
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May develop lupus syndrome (33%)
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Procainamide
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Ideal drug to treat ventricular arrhythmias
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Lidocaine
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Unlike quinidine, this drug blocks both activated and inactivated Na+ channels
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Lidocaine
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DOC for treating digoxin-induced arrhythmias
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Lidocaine
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Similar to lidocaine, this drug is reserved for treatment of arrhythmias, otherwise not responsive to treatment
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Flecainide
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Similar to lidocaine and Flecainide, this drug may precipitate life-threatening arrhythmias
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Propafenone
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Beta-blocker which increases AP duration similar to class III antiarrhythmics
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Sotalol
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Class II antiarrhythmic mechanism
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Prolong phase 4 depolarization
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Esmolol
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beta-blocker which is rapidly metabolized
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Unique class III antiarrhythmic which blocks Na, K, and Ca channels
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Amiodarone
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Antiarrhythmic which may cause thyroid problems (5%)
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Amiodarone
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Selective K-channel blocker
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Dofetilide
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Selective K-channel blocker which may induce Torsade de Pointes
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Prolongs QT interval
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DOC for treatment of superventricular tachycardia
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Verapamil (depress AV-nodal conductance)
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Ca++ channel blocker with less negative inotropic effects than verapamil
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Diltiazem
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Converts paroxysmal supraventricular tachycardia
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Adenosine
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Rapid activation of Kir channels causing hyperpolarization and suppression of Ca++ channels
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Adenosine
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Used to treat Torsade de Points
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Magnesium
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