Pharmy 3

Front 1

acetazolamide

Back 1

carbonic anhydrase inhbitors, act mainly in proximal tubular epithelial cells, less efficient than others, used for its pharmacological properties, applications- galucoma, epilepsy, moutain sickness, metabolic alkalolosis, MOA- inihibts intracellular carbonic anhydrase, decreases ability to exchange Na for K, HCO3 retianed in lumen, oral and well absorbed, half life- 3-6h, adverse- metabolic acidosis, hyponatremia, hypokalemia, crystalluria, malaise, fatigue, depression, head ache, GI distrubances, drowsiness, paresthesia

Front 2

mannitol

Back 2

osmotic, raises ostomic pressure of plasma drqing H20 out of body tissues and producing ostmotic duiresis, does not effect Na excretion, clinical- increase urine flow in pts with acute renal failure, reduce increased intracranial pressure and tx of cerebral edema, promote excretion of toxic suvstances , IV, extracellular water expansion, tissue dehydration

Front 3

conivaptam

Back 3

ADH antagonist, V1 and V2 antagonist, diluted urine, used for euvolumeic or hypervolmeic hyponatremia, SIADH, hrt failure, MOA- antagonizes effects of ADH, IV only, 5 hrs, metabolized and potent inhbitor of CYP 3A4 , adverse-infusion site reaction, thrist, atrial fibrliaation, GI, electrolyte distrubances, nephrogenic diabetes insipidus

Front 4

captopril

Back 4

ACE inh, fist line agents agaisnt HTN, MOA- decrease BP by decreased peripheral vascular resistant, do not reflexibly increase CO, rate or constractility, inhibit ACE, decrease Na and H20 retension, increase bradykinin levels , clinical app- HTN drug most effective maong white and young pts, preserve renal function in diabetic or non diabetic nephrapy, good for diabests, tx of chronic HF, standard care following MI , started 24h after end of infraction adverse- dry cough, hypotension, hyperkalemia, rash, fever, alterd tase, angioedmia, acute renal failure, contraindictions-pregancy, bilat renal artery stenosis

Front 5

enalpril

Back 5

ACE inh, fist line agents agaisnt HTN, MOA- decrease BP by decreased peripheral vascular resistant, do not reflexibly increase CO, rate or constractility, inhibit ACE, decrease Na and H20 retension, increase bradykinin levels , clinical app- HTN drug most effective maong white and young pts, preserve renal function in diabetic or non diabetic nephrapy, good for diabests, tx of chronic HF, standard care following MI , started 24h after end of infraction adverse- dry cough, hypotension, hyperkalemia, rash, fever, alterd tase, angioedmia, acute renal failure, contraindictions-pregancy, bilat renal artery stenosis

Front 6

lisinopril

Back 6

ACE Inh, fist line agents agaisnt HTN, MOA- decrease BP by decreased peripheral vascular resistant, do not reflexibly increase CO, rate or constractility, inhibit ACE, decrease Na and H20 retension, increase bradykinin levels , clinical app- HTN drug most effective maong white and young pts, preserve renal function in diabetic or non diabetic nephrapy, good for diabests, tx of chronic HF, standard care following MI , started 24h after end of infraction adverse- dry cough, hypotension, hyperkalemia, rash, fever, alterd tase, angioedmia, acute renal failure, contraindictions-pregancy, bilat renal artery stenosis

Front 7

aliskiren

Back 7

"inhibits enzyme acitivty of renin and prevents concersion of angiontesnogen to ang I-->inhibits production of angiotensin II and aldosterone adverse- ,GI distumrabes, hypotension, hyperkalema, renal impairmen, angioedema , contradincated in pregnacy

Front 8

losartan

Back 8

ARB, altnerative to ACE inhbitorys, blocks ang II type I receltors, MOA- decrease BP by causing arlteirolar and venous dilatation, block aldosterone secretion-->decreases Na and H20 retention, do not increase bradykinin levels, decrease diabetic nephrotoxicity(attractive therapy in hypertensive diabetics), adverse effects- dry cought DOES NOT occur, no effect on bradykinin, less rsik of angiodema, contraindictions- pregancy and bilat renal artery stenosis

Front 9

valsartam

Back 9

ARB, altnerative to ACE inhbitorys, blocks ang II type I receltors, MOA- decrease BP by causing arlteirolar and venous dilatation, block aldosterone secretion-->decreases Na and H20 retention, do not increase bradykinin levels, decrease diabetic nephrotoxicity(attractive therapy in hypertensive diabetics), adverse effects- dry cought DOES NOT occur, no effect on bradykinin, less rsik of angiodema, contraindictions- pregancy and bilat renal artery stenosis

Front 10

amlodipine

Back 10

calclium channel blocker, first line agent agaisnt HTN, effective for angina or diabetc pts, high doses can increase tisk of MI(excessive casoldiation and reflex cardiac stimualtion) , least sekectuve, effects on cardiac and smooht muscle, used to tx angina, supraventricular tachyarrthmias and migraine MOA- Ca blcoekrs bind to L type Ca channels in hrt and smooth muscle of peripheral vasuclar and hrt, Ca entry blocked-->vascular smoohth msucle relaxation and arteriolar dilation-->decrease BP , no need for directic, safe in pts with asthma diabetest, peripheral vascualr diecrase, oral, short half life- 3-8h, adverse- hypotension, dizziness, head ache, fatigue, peirpheral edema(feet and ankles) bradycardia, hrt block

Front 11

nifedipine

Back 11

calclium channel blocker, first line agent agaisnt HTN, effective for angina or diabetc pts, high doses can increase tisk of MI(excessive casoldiation and reflex cardiac stimualtion) , least sekectuve, effects on cardiac and smooht muscle, used to tx angina, supraventricular tachyarrthmias and migraine MOA- Ca blcoekrs bind to L type Ca channels in hrt and smooth muscle of peripheral vasuclar and hrt, Ca entry blocked-->vascular smoohth msucle relaxation and arteriolar dilation-->decrease BP , no need for directic, safe in pts with asthma diabetest, peripheral vascualr diecrase, oral, short half life- 3-8h, adverse- hypotension, dizziness, head ache, fatigue, peirpheral edema(feet and ankles) bradycardia, hrt block

Front 12

verapamil

Back 12

calclium channel blocker, first line agent agaisnt HTN, effective for angina or diabetc pts, high doses can increase tisk of MI(excessive casoldiation and reflex cardiac stimualtion) , least sekectuve, effects on cardiac and smooht muscle, used to tx angina, supraventricular tachyarrthmias and migraine , MOA- Ca blcoekrs bind to L type Ca channels in hrt and smooth muscle of peripheral vasuclar and hrt, Ca entry blocked-->vascular smoohth msucle relaxation and arteriolar dilation-->decrease BP , no need for directic, safe in pts with asthma diabetest, peripheral vascualr diecrase, oral, short half life- 3-8h, adverse- constripaiton, avoid in CHF due to negative inotropic effects

Front 13

hydralazine

Back 13

tx hypertensive emergenies in pregnancy related to eclemspia

Front 14

minoxidil

Back 14

direct vasodilater, direct acting smooth muscle relazes, refelx tacycahria, increased plasma remini, SE blocked if combised with duirects or B1 blockers, direct periphjeral vasodilation of arterioles, oral tx of severe-malignant HTN, adverse- reflex tachycardia and fluid retension, male pattern baldness(hypertricohosis)

Front 15

nitroglycerin

Back 15

arterial and venous vasodilater, used for hypertenve pts with cardiac ischmea or angina, post cardiac bypass surgery, 2-5 min half life

Front 16

fenoldopam

Back 16

preipheral dopamine-1 receptor agonist, arteriolar dilation, IV infusion for hypertnesive mergency, mainatains or increases renal perfusion as lowers BP, promotes naturesis, jalf life- 30 min, safe to use in all hypeernteiv emergencies particularsly renal insufficiently, contraindictions- glaucoma

Front 17

Nicardipine

Back 17

calcium channel blocker, IV infusion of hypertensive emergency, half life- 30 min, reflex tachycardia

Front 18

Sodium Nitroprusside

Back 18

DOC for hypertensive emergneycies, IV, prompt vasoldiation and reflex tachycardia, half life- 1-2 min- requires continous infusion, adverse effects- hypotension(overdose), goose bumps, abd cramping, nausea, vomting, head ache, metabolism--> cyanide ion, toxicity rare but can be treated with sodium thiosulfate infusion-->thiocynate excreted from body not toxic

Front 19

Hydralazine

Back 19

direct vasodilater, direct acting smooth muscle relazes, refelx tacycahria, increased plasma remini, SE blocked if combised with duirects or B1 blockers, acts on arterioles, tx pregnacy induced HTN, management of HTN in last line of therapy , oral or IV, IV for hypertensive crisis, adverse- edema, reflex tachycardia, HA, nausea, sweating, flushing, adminsiter with thazie or B blockrs to combat reflex tachycardia and fluid retention

Front 20

Bosetan

Back 20

nonselextive receptro blockers, blocks both intial transient depressor ETA and prolonged pressor ETB responses to IV endothelin, pregnacy-category X , inibits endothelin sysntesis and actions

Front 21

Candesartan

Front 22

inamrinone

Front 23

digoxin

Back 23

shortens refractory period in atrial and ventnricualr myocardial cells, prolongs effective refractory period and diminishes coudnction velocity in AV node, clinical app- control of ventricular response rate in atrial fibirlalation and flutter with impaired LV function or hrt failure, adverse- toxic dose- ectopic ventricular beats-->ventricualr tachycardia and fibrillation , heart failure0 psotive ionontripe, arrthimas-direct AV node blocking effects and vagomimetic properties- inhbition of Ca currents in AV node, activation of Ach mediated K currents in atrium, major indirect actions- hyerpolarization, shortening of atrial action potentials, increases in AV nodal refractoriness, show AV conduction and prolongs the efective refractory period of AV node and decreases the fraction of atrial impluses that are conducted through the node, useful in treating atrial flutter/fibirllations(controlling ventricualr rate)

Front 24

glucagon

Front 25

milrinone

Front 26

Disopryamide

Back 26

class IA antiarrthmic, slow rate of change of depolaziation phase(0) of action pontetion(slowing coudnciton) prolonging AP and increasing ventricualr effective refractory period, prolong repolaziation phase(3) by an effect on K channels, intermiedate speed of association-inactivated Na channels and intermediate rate of dissociation , MOA- negtive ionotripic effect, antimustaic properties, causes peripheral vasoconstriciton, blocks K channels(Class III), clinical app- supraventricular and ventricualr arrhythmias, pharmokinetics- excreted unchanged by kidnye, convereted in liver(CYP 3A4), adverse effects- pronounced negative ionotripic effects, may induce hypotension and cardiac failure without preexisting myocardial dysfunction, severe antimuscarinic effects(dry mouth, urinary retention, blurred vision, constipation)

Front 27

Procainamide

Back 27

class IA antiarrthmic, slow rate of change of depolaziation phase(0) of action pontetion(slowing coudnciton) prolonging AP and increasing ventricualr effective refractory period, prolong repolaziation phase(3) by an effect on K channels, intermiedate speed of association-inactivated Na channels and intermediate rate of dissociation , MOA- derivative of local anesthenic procaine, slimilar actions to quinidine. blockage of Na channels in activated state, blockage of K channels, antimuscarinic properties , clinical ap- ventricualr arrthmias, reserved for life threatining arrthymias, pharmokinetics- oral, well absorbed, t- 2-3h, NAPA elecimated by kidney, metabolized by CYP2D6 , adverse- chronic use- high incidence of AE, toxic doses- asystole, induction of ventricualr arrythmias, CNS effects(depression, hallucination, psychosis), GI intolerance less frequent with quinidine, hypotension , contraindications- hypersensitivty, complete hrt block, 2nd degree AV block, SLE, torsades de poitnes, heart failure and hypertnesion

Front 28

Quinidine

Back 28

class IA antiarrthmic, slow rate of change of depolaziation phase(0) of action pontetion(slowing coudnciton) prolonging AP and increasing ventricualr effective refractory period, prolong repolaziation phase(3) by an effect on K channels, intermiedate speed of association-inactivated Na channels and intermediate rate of dissociation , concominant class III avitility(block K channels) can precipitate arrythmias) due to toxicity is being replaced by Ca antagonists, clinical app- conversion and presention of relapse into atrial fibirllation and or flutter, suppresion of ventricualr arrythmias, replaced by more effectve/safer antiarrhythmic agents , mOA- prevents Na influx, slows phase 0, decreases slope of phase 4, inhibits K channels, pharmokinetics- quinidine sulfate- rapid oral absoprtion, forms active metabolite CYP3A4, inhibits CYP2D6, 3A4, and P glycoprotein , adverse- arrythmias, SA and AV blocks or aystole, nausea, vomting, and diarrhea. thrombocytopenic purpura, toxic doses- ventricular tachycardia, cinchonsim( blurred vision, tinnitus, head ache, psychosis), mixed alpha- adrenergic block and antimuscarinic properties, can increase(digoxin by decreasoing renal clearance , contraindications- do not use in pts with complete hrt block, extreme caution with prolonged QT interval, hx of torsades de pointes, incomplete hrt block, uncompensated hrt failure, myocarditis, severe myocardial damange

Front 29

Lidocaine

Back 29

class I B antiarrthmic, little effect on depolaziation phase of action potential in normal cells(more selctive effect in ischmeic or diseased tissue) decrease duration of AP by shortening repolaizaion, rapidly interact with Na channels, local anesthenic, rapidly asociates and dissociates from Na channels, actions manifest when cells are depolrizaed or firing rapidly(more effect on ischemic or deicreased issue) parotuclarly useful in treating ventricualr arrthmias, little effect on K channels, MOA- shortens phase 3 repol, decreases duration of AP, clinical app- DOC for termination of ventricualr tachycarida and prevention of ventricular fibrillation after cardioversion in setting of acute ischemia , little effect on atrial or AV junction arrthythmias , IV only, metablized by liver-first pass metabolism , adverse- wide toxic therapetic ratio, little impairment of LV function, no negative ionotric efect, CNS effects, cardiac arrthmias, toxic doses- convulsions, coma

Front 30

Mexiletine

Back 30

Class IB antiarrthmic, orally active derivative of lidocaine, management of severe vetnricualr arrthmias(used oraally and IV), mainly CNS and GI adverse effects

Front 31

Tocainide

Back 31

Class IB antiarrthmic, orally active derivative of lidocaine, tx of ventricualr tachyaryhmias, used orally and IV, severe hematological and pul toxicity(limits use)

Front 32

Flecainide

Back 32

class IC arrthmic, markedly depress rate of change of depolarziation pahse action potential--> marked slowing of coduction of action potential, ltitle effect o nduration or ventricualr effective refractory period, bind slowly to NA channels, slowly dissociates from resting Na channels, show prominent effects even at normal HR, MOA- decreases rate of rise of Phase 0 depolarziation without affecting duration of AP, causes slight prolongoation of refractory periods, automacially reduced by an increase in threshold potential of ventricle rather than decrease in slope of phase 4 , severe sympathetic ventricualr arrhytymias( life threatening only) premature ventricular contraction or ventricular tachycardia resitant to other therapy, severe symptomatic supraventicualr arrhthmias and prevention of paroxysmal atral fibrillation, increased mortality more than two fold post MI pts treatesd for poreamture contractions(CAST), oral, half life 16-20h. adverse- aggravates CHF, CNS effects- dizziness, blurred vision, head ache, nausea, vomiting, diarrhea, arrythmias and ventriicualr tachycarida

Front 33

Propafenone

Back 33

class I C arrythmic, MOA- decreases rate of rise in Phase O depolaiztion without affecting duration of AP, prologns coudnction and refarcotirness in all areas of myocardium, prolongs effective refractory period and reduces spontaneous automaciltiy, clinical app- used for tx of life threatneing ventricular arrhytmias and maintanence of normal sinus rhythm in pts with ysmptomatic atrial fibrillation

Front 34

amiodarone

Back 34

class III antiarrthmic, clinical app- commonly used, mamangent of ventricualr and supraventricular arrhytmias, low dose- matianing normla sinus rhythm in pts with atrial fibrillation

Front 35

dofetilide

Back 35

class III, clinical app- maintaince of normal snius rhythm in pts with chronic atrial fibirllation and flutter of longer than 1-week duration who have been converted to normal sinus rhythm, conversion of atrial fibiraltion and fluuter to normal sinus rhythm, half life- 10 hr, excreted in urine

Front 36

sotalol

Back 36

Class III, antiarthmic drug, potent non selective B blocker, MOA- inhibits rapid outward K current(delayed rectifier), prologns repolaziation and duration of AP, lengthens refractory period(class III activity), clinical app- tx of life threatening ventricualr arryhtmias, maintenece of sinus rhythm in pts with atrial fibrillation and flutter who are currently in sinus rhythm

Front 37

adenosine

Back 37

naturally occuring nucleoside(P1 receptor agonist), high doses- decreases conduction velocity and prolongs refractory period as well as decreasing automaticity in AV node, very short half life- 15s, MOA- enhances K conducatance, inhibits cAMP mediated Ca influx, hyperpolarization in AV node

Front 38

magnesium

Back 38

functional Ca antagonist, antiarrthmic, used for torades de ppoitnes, digitalis induced arthmia,prophylaxis of arrhythmia in acute MI

Front 39

heparin

Back 39

drug therapy for atrial fibrilaation, prevention of htrombolytic event, unstable pts who require immediate cardioversion(give IV)

Front 40

warfarin

Back 40

drug therapy for atrial fibrilaation, prevention of htrombolytic event, in stable pts cardioverison sould be delayed 3-4 weeks unti adequate anticoag acheiced, oral