Quiz 1 Material Flashcards
Propranolol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Nitroprusside
Parenteral Agents MOA: Causes release of NO with result of increased intracellular cGMP and dilates arterioles and veins
Amlodipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Dopamine
Inotropes (Beta-adrenergic agonists) MOA: Cause positive inotropic effects and vasodilation; increase cAMP which activates protein kinase, and protein kinase increases calcium influx into cells
Acetazolamide
Carbonic Anhydrase Inhibitor MOA: Prevent carbonic anhydrase from catalyzing the reaction that form bicarbonate and decrease the kidney’s ability to exchange Na for H
Mannitol
Osmotic Diuretics MOA: Filtered through the glomerulus and carries water with them
Metoprolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Moexipril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Isosorbide mononitrate
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
Prazosin
Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP
Ethacrynic acid
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
Bisoprolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Milrinone
Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation
Enalapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Diltiazem
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Methazolamide
Carbonic Anhydrase Inhibitor MOA: Prevent carbonic anhydrase from catalyzing the reaction that form bicarbonate and decrease the kidney’s ability to exchange Na for H
Acebutolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Fenoldopam
Parenteral Agents MOA: Peripheral dopamine-1 receptor agonist Relaxes mainly the renal and mesenteric arterial vessels and increases renal blood flow
Eprosartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Hydralazine
Vasodilators MOA: Releases NO
Isosorbide dinitrate
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
Bumetanide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
Esmolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Nitroglycerin
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
Benazepril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Felodipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Ranolazine
Sodium (NA) Channel MOA: Inhibits the late phase of the Na current, and reduces intracellular sodium and calcium overload Improves diastolic function
Dobutamine
Inotropes (Beta-adrenergic agonists) MOA: Cause positive inotropic effects and vasodilation; increase cAMP which activates protein kinase, and protein kinase increases calcium influx into cells
Indapamide
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
Irbesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Labetalol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Clonidine
Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release
Azilsartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Trandolapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Verapamil
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Valsartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Captopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Telmisartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Nisoldopine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Quinapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Clevidipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Chlorthalidone
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
Doxazosin
Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP
Ramipril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Cilazapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Atenolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Carvedilol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Nebivolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Nicardipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Metolazone
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
Isradipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Epleronone
Potassium-Sparing Diuretics MOA: Act on the collecting tubule/duct; Blocks aldosterone receptors and prevents production of proteins that stimulate Na/K exchange sites of the collecting tubules
Minoxidil
Vasodilators MOA: Hyperpolarizes smooth muscle by opening potassium channels
Inamrione
Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation
Aliskiren
Renin Inhibitor MOA: Directly inhibits renin
Terazosin
Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP
Fosinopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Spironolactone
Potassium-Sparing Diuretics MOA: Act on the collecting tubule/duct; Blocks aldosterone receptors and prevents production of proteins that stimulate Na/K exchange sites of the collecting tubules
Furosemide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
Nifedipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
Digoxin
Inotropes (Cardiac glycosides) MOA: Inhibits the ability of the monocyte to actively pump Na from the cell
Hydrochlorothiazide (HCTZ)
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
Lisinopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Torsemide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
Nadolol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
Perindopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
Losartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Olmesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
Methyldopa
Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release
Candesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels