Therapeutics test 1 drugs – Flashcards

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Hydrochlorothiazide
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thiazide diuretic
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chlorthalidone
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thiazide diuretic
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Indapamide
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thiazide diuretic
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metolazone
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thiazide diuretic
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furosemide
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loop diuretic
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bumetanide
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loop diuretic
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torsemide
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loop diuretic
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ethacrynic acid
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loop diuretic
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amiloride
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potassium sparing diuretic
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triamterene
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potassium sparing diuretic
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spironolactone
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potassium sparing diuretic
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glycerol
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osmotic diuretic
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mannitol
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osmotic diuretic
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acetazolamide
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carbonic anhydrase inhibitor- diuretic
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propranolol
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non selective Beta blocker
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Timolol
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non selective beta blocker
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nadolol
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non selective beta blocker
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metoprolol
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selective b1 blocker
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atenolol
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selective b1 blocker
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bisoprolol
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selective b1 blocker
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betaxolol
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selective b1 blocker
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acebutolol
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selective beta1 blocker with ISA (agonistic effect for mostly b1)
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penbutolol
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non selective beta blocker with ISA
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pindolol
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non selective beta blocker with ISA (greater partial agonist for B2 than B1)
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carvedilol
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non selective beta blocker and selective a1 blocker
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labetalol
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non selective beta blocker with partial agonistic activity for B2 and selective a1 block
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nebivolol
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selective beta1 blocker with NO vasodilating effect
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captopril
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ACE- inhibitor (sulfhydryl containing)
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fosinopril
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ACE inhibitor (phosphonate-containing)
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Enalapril (enalaprilat), benazepril, lisinopril and quinapril
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ACE inhibitors (dicarboxylate containing)
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Losartan, Candesartan, irbesartan, valsartan, telmisartan, eprosartan
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Angiotensin 2 receptor blockers (ARBs)
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Aliskiren
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Renin inhibitor
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Verapamil
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non-dihydropyridine L-type calcium channel blocker
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Diltiazem
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non-dihydropyridine L-type calcium channel blocker
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Nifedipine
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Dihydropyridine L-type calcium channel blocker
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Amlodipine
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Dihydropyridine L-type calcium channel blocker
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felodipine
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Dihydropyridine L-type calcium channel blocker
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hydralazine
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Vasodilator
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Minoxidil
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Vasodilator
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Nitroprusside
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vasodilator
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methyldopa
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centrally acting a2 agonist
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clonidine
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centrally acting a2 agonist (diagnoses phenochromocytoma)
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guanabenz
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centrally acting a2 agonist
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guanfacine
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centrally acting a2 agonist
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guanadrel
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adrenergic neuron blocker
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guanethidine
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adrenergic neuron blocker
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metyrosine
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tyrosine hydroxylase inhibitor (inhibits synthesis of NE)interferes with sympathetic neuron function
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reserpine
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inhibits storage of catecholamines into vesicles interferes with sympathetic neuron function
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prazosin
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selective a1 blocker
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terazosin
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selective a1 blocker
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doxazosin
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selective a1 blocker
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phenoxybenzamine
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non selective a blocker
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phentolamine
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non selective a blocker
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treprostinil
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new anti htn agent, prostacyclin analogue
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tadalafil
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new htn agent, pde inhibitor
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Thiazide MOA
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inhibits na+/cl- pump on luminal side of DCT (short term: dec CO by dec blood volume) long term: dec sodium in SM= dec sensitivity to vasopressors= dec PVR= dec BP)
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Loop Diuretics MOA
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inhibit Na+/Cl-/K+ cotrans on apical side of TAL. (dec BV= dec preload= dec. SV= dec CO= dec BP).

also stimulates renin release by blocking TGF by blocking sodium from entering macula densa
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Potassium sparing diuretics (spironolactone) MOA
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blocks the binding of aldosterone in the collecting duct which decreases sodium and increases K+ and H+
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K+ sparing diuretics (amiloride and triamterene)
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blocks na+ channel on apical side of late DCT
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Osmotic diuretics MOA
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increases osmotic pressure of plasma, (mannitol not reabs), reduces conc. grad of sodium which decreases reabs of sodium.
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Carbonic anhydrase inhib MOA
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inhibits reabs of sodium bicarb. acts at PCT. increases acidity of blood
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non-selective beta blockers MOA
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blocks NE effects by binding to b1 and b2 receptors (decreases contractility=dec SV= dec CO= dec BP) (dec HR= dec CO= dec BP) BLOCK RENIN RELEASE (inhib Gs in Juxt cells which dec Camp and dec renin release) at first inc PVR but in long term dec.
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selective b blockers MOA
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more affinity for B1 than B2. (block NE action, dec CAMP= dec ca levels= dec contractility= dec CO= dec HR) DECREASE HR and CONTRACTILITY. BLOCK RENIN RELEASE
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Beta blockers w/ ISA MOA
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less likely to cause lowered HR and cold extremeties. Decreases CO but doesn't lower contractility or HR as much b/c ISA calms those effects
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combined a and b blockers MOA
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blocking a 1 receptor= vasodilation
dec HR and contractility (B1 block) dec PVR ( a1 block)
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B blocker w/ NO vasodilating MOA
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causes release of NO by binding to B 3 recep on vasculature
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ACE inhib MOA
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inhib ACE conversion of Ang 1 to Ang 2 therefore inhibiting Angiotensin 2 action (vasoconstrictor) causing vasodilation. and blocks aldosterone (dec BP) Dec arteriole and venous pressure, dec sodium inc. in potassium and dec cardiac afterload= inc CO (compensatory)
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ARB MOA
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block angiotensin 2 AT1 receptors
- relax SM= vasodilation= inc H2o and sodium excretion= dec in BV
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REnin inhib
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block angiotension conversion to ang 1
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non-dihydropyridine cach block MOA
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blocks ca channels in heart and vasculature (sM)
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dihydropyridine MOA
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block ca channels in BV causing vasodilation on arteriol side dec hr and contractility
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Hydralazine MOA
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relaxes arteriolar SM (dec SVR= dec BP)
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Minoxidil MOA
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PRODRUG

activates Katpase channel so lets K+ out of cell to relax
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nitroprusside MOA
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releases NO which vasodilates (inc cgmp dec SVR dec BP
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Centrally acting alpha 2 agonists MOA
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bind to a 2 receptor which increase PNS outflow and inc vagal outflow which dec. arteriole and venous tone
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adrenergic neuron blocker MOA
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drug taken up into neuron by uptake 1 (at postganglionic presynaptic nerve terminal) and replaces NE in vessicles and lets it be eaten up by MAO
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metyrosine MOA
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block production of NE by stoping tyrosine hydroxylase dec NE dec BP
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reserpine MOA
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block packagine of NE, DA and seritonin into secretory vesicles and lets it leak into cytosol and be eaten by MAO
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selective alpha 1 blockers MOA
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block alpha 1 postsynaptically which inhibits vasoconstriction lowering BP. reduce arteriole tone/resistance and dilates venous side (dec CO)
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non-selective alpha blockers
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a1 in postsyn cell membrane and a2 in presyn nerve terminal. dec PVR and dec BP. venodilators!!!
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