drugs Flashcards
(61 cards)
<p class=”large” style=”text-align:center”;>propranolol</p>
<p class=”large” style=”text-align:center”;>non selective beta blocker
high lipid solubility
eliminated by liver</p>
<p class=”large” style=”text-align:center”;>atenolol</p>
<p class=”large” style=”text-align:center”;>beta 1 selective beta blocker
low lipid soluble
eliminated by kidney
longer action –> can be dosed once daily
class II antiarrhtyhmic</p>
<p class=”large” style=”text-align:center”;>what are class I and III antiarrhythmics used for</p>
<p class=”large” style=”text-align:center”;>vent tachy
atrial fib
AV reentry</p>
<p>carvedilol</p>
non selective beta blocker with alpha 1 activity
especially useful for congestive heart failure
moderate lipid solubility
eliminated by liver
labetolol is another combination blocker</p>
<p>metoprolol</p>
beta 1 selective beta blocker
with moderate lipid solubility
eliminated by liver</p>
<p>atropine</p>
parasympathetic antagonist (muscarinic) competitive antagonist
blocks vagal response
might stop AV block –> for ex inferior wall MI or dig toxicity
almost no CNS effect at clinical doses
given by IV</p>
<p>procainamide</p>
class Ia antiarrhythmic
tragets Ina and Ik
depresses fast response excitability and increases APD</p>
<p class=”large” style=”text-align:center”;>lidocaine</p>
<p class=”large” style=”text-align:center”;>class Ib antiarrhythmic
Targets Ina
depresses fast response excitability especially in depolarized tissue
*not useful at normal resting potential</p>
<p>flecainide</p>
class Ic antiarrhythmic depress fast response excitability in noemal and depolarized tissue</p>
<p class=”large” style=”text-align:center”;>dofetilide</p>
<p class=”large” style=”text-align:center”;>class III antiarrhythmic
targets Ik
prolong APD without depressing excitability in fast response tissue</p>
<p>verapamil</p>
Ca cahannel blocker
Ica targeted
depress conduction and excitability in slow response tissue (AV node, SA node)
effective in tx of paroxysmal SVT and tx of angine (decrease myocardial o2 demand and increase coronary blood flow) & tx htn (reduce SVR)
*notable side effect is constipation</p>
<p>what are class I and III antiarrhythmics used for</p>
vent tachy
atrial fib
AV reentry</p>
<p class=”large” style=”text-align:center”;>factors that modify the strength of sodium channel blockade</p>
<p class=”large” style=”text-align:center”;>Ib< IA< IC
resting membrane potential - more potent when more negative
hear rate - more potent at faster heart rate</p>
<p class=”large” style=”text-align:center”;>what are class IV antiarrhythmics, digoxin and adenosine used for</p>
<p class=”large” style=”text-align:center”;>AVNRT</p>
<p>what is unique about class Ia antiarrhythmic</p>
also blocks Ik so increased action potential duration</p>
<p class=”large” style=”text-align:center”;>factors that modify the strength of sodium channel blockade</p>
<p class=”large” style=”text-align:center”;>Ib< IA< IC
resting membrane potential - more potent when more negative
hear rate - more potent at faster heart rate</p>
<p class=”large” style=”text-align:center”;>selectivity of calcium channel blockers</p>
<p class=”large” style=”text-align:center”;>verapamil - cardiac
nifedipine - vascular
diltiazem cardiac and vascular</p>
<p>factors that increase the effect of Ik blockade on APD</p>
slow hear rates
low extracellular K
low extracellular M</p>
<p>effect of digoxin in arrhythmia</p>
enhance vagal by increasing muscarinic receptor
decress I ca and increase I K ach
*only drug that acts on slow response tissue that is a positive inotrope
slow onset of effect and duration greater than 1 day!</p>
<p>adenosine</p>
adenosine receptor agonist
decrease calcium current and icnrease potassium current from ach
onset of action and duration of effect is seconds!!</p>
<p class=”large” style=”text-align:center”;>what is major determinant of ERP in fast and slow response tissue?</p>
<p class=”large” style=”text-align:center”;>fast - APD
slow- recovery of ca channel</p>
<p class=”large” style=”text-align:center”;>selectivity of calcium channel blockers</p>
<p class=”large” style=”text-align:center”;>verapamil - cardiac
nifedipine - vascular
diltiazem cardiac and vascular</p>
<p class=”large” style=”text-align:center”;>prazosin</p>
<p class=”large” style=”text-align:center”;>alpha 1 & alpha 2 antagonist - alpha 1 more than alpha 2
used to decrease peripheral vascular resistance
primary used in tx of htn (third line)
improves voiding in pts with urinary bladder outlet obstruction
postural hypotension may occur</p>
<p class=”large” style=”text-align:center”;>how to tx afib</p>
<p class=”large” style=”text-align:center”;>1) slow AV node -> atenolol, digoxin, verapamil
2) stop fibrillation in atrial muscle –> procainamide, amiodarone, sotalol, dofetilide, dlecainide</p>
conditions that raise risk of using antiarrhythmic drugs
prolonged QT esp with low K, Mg sick sinus node AV block poor systolic fx
prazosin
alpha 1 & alpha 2 antagonist - alpha 1 more than alpha 2 used to decrease peripheral vascular resistance primary used in tx of htn (third line) improves voiding in pts with urinary bladder outlet obstruction postural hypotension may occur
how are beta blockers used in CV medicine
decrease HR, decrease impulse conduction, decrease cardiac contractility and metabolic rate used in heart failure, MY/angina, arrhythmias, htn
alpha adrenergic antagonists
prazosin, doxazosin, terazosin zosin endings! Doxa and tera are pura alpha 1 blockers doxa and tera are slower onset and longer duration
beta adrenergic antagonists
propranolol, metoprolol, atenolol, carvedilol distinguished by beta 1 selectivity, instrinsice sympathomimetic activity, lipid solubility duration of action atenolol- hydrophilic- metabolized by kidney
ends for sympathetic antagonists & ace inhibitors
beta antagonists - end with olol or ilol alpha ends with zosin ace inhibitor - pril
selectivity of beta blockers
propranolol - beta 1 & 2 - nonselective metoprolol & atenolol - beta 1 selective carvedilol - non-selective with alpha 1 blockade!
how are beta blockers used in CV medicine
decrease HR, decrease impulse conduction, decrease cardiac contractility and metabolic rate used in heart failure, MY/angina, arrhythmias, htn
name ace inhibitors
captopril enalapril lisinopril rampipril
other enzymes that can make ang II
CAGE cathepsin G chymase from angiotensinogen --> angII t-Pa cathepsin G tonin
arbs
block AT1 downstream from alternative angII pathway no build up of bradykinin (good & bad) AT2 receptors still are able to be acivated
thiazide
diuretic acts at distal convoluted tubule by binding to NaCl cotransporter and reducing Na absorption reduces blood volume and decreases CO and BP compensatory mechanisms counteract the acute effects LT (renin and aldosterone) variable degree of adaptation mechanism of LT action mystery --> proposed decrease in PVR secondary to increased NO production long duration fo action (24 hours)
two classes of calcium channel antagonists
1) non dihydropyridine --> verapamil, diltiazem 2) dihydropyridines--> nifedipine, amlodipine non-dihydro- bind while channel is open --> more effective in tissue that is frequently stimulated dihyrdo- bind during resting state
direct peripheral vasodilators
venous - nitrates arterial hydralazine, minoxidil both arterial and venous - nitroprusside don_t share common MOA use second drug to block compensatory mech (beta blocker often)
minoxidil
direct vasodilator that activates atp-modulated K[ channel in arteris allowing k+ to leave cell cause hyperpolarization and relaxation direct arteriolar vaso without effect on veins decrease in pvr --> lower bp use with b blockers and diuretics to stop compensatory mech
beenfits of beta blockade in tx of ischemia
improve myocardial o2 supply --> decrease hr which prolongs diastole, improves subendocardial perfusion decrease myocardial o2 demand --> suppresses HR & contractility, blocks sympathetic reflex, reduces double product, helps reduce BP
losartan
first synthetic antagonist to AT1 receptor
limitations of ace inhibitors
non specific enzyme alternate pathways for ang II poor side effect profile - cough and rare angioedema
direct renin inhibitor
inhibits renin at pt of activation by binding to renin increases plasma renin concentration reduces production of angI, angIII and PRA less potent than acei and arbs are monotherapy aliskiren - $$
toxicities of thiazide diuretics
sulfa allergy hypokalemia promote insulin resistance increase TG and LDL cholesterol
diltiazem
non dihydropyridine CCA --> lowest incidence of SE and effective in tx SVT not great htn drug
nifedipine
CCA that is primarily peripheral vasodilatory effects effective for atn contraindicated in post MI, CNF bc fine balance of o2 demand --> result in increase hr because of profound decrease in PVR side effects - facial flushing, headaches, dizziness, palpitations most commonly prescribed anti htn drug as monotherapy
hydralazine
unknown moa direct arteriolar dilation with no effect on veins preferentially effects renal, peripheral, splanchnic and coronary arteirs descrease in pvr --> decrease BP SE - flushing, sweating, palpitations, hypotension, angina **phase 2 metabolism --> acetylation **limited use - hypertension during pregnancy including preeclampsia usually used in combo with b antagonist
minoxidil
direct vasodilator that activates atp-modulated K[ channel in arteris allowing k+ to leave cell cause hyperpolarization and relaxation direct arteriolar vaso without effect on veins decrease in pvr --> lower bp use with b blockers and diuretics to stop compensatory mech
mechanism of action of centrally acting alpha 2 adrenergic agonist
stimulate pregangionic alpha 2 receptors on adrenergic neurons in medullar --> reductes sympathetic outflow creating unopposed vagal tone decrease PVR, HR, CO and BP methyldopa & clonidine
tx of htn for isolated systolic htn
diuretics reduce strokes
sodium nitroprusside
MOA - metabolized by smc into NO --> activates guanylate cyclase --> c-GMP which produces SMC relaxation and vaso -both arterioles and veins --> decrease pre and after load *rapid metabolized in rbcs in to cyanide which is metabolized by rhodanase in mito to thiocyanate dosium thiosulfate, cofact for shodanase, is added to solution prior to administration to prevent cyanide tox unstable in direct sunlight **used for htn emergencies - rapid onset 1 - 2 minutes and everyone responds initiate therapy with b blocker before discontinuing infusion
reserpine
1st drug to tx htn depletes peripheral NE from storage vesicles in sympathetic nerve endings --> decrease PVR takes 2-3 weeks for max effect SE - depression
centrally acting alpha 2 adrenergic agonist
methyldopa clonidine
tx of htn post mi
Beta blocker acei Aldosterone agonist
tx of htn with dbm
diuretic aci arb cca
tx of htn for isolated systolic htn
diuretics reduce strokes
amiodarone
class III antiarrhythmic that prolongs phase 3 of cardiac AP but has other effects similary to class Ia, II and IV -- show beta blocker-like and potassium channel blocker-like actions on SA and AV nodes txs both acute life-threatening arrthmias and chronic suppresion of arrhythmias both SV and V arrthymias
rational use of anti htn drugs in combo
diuretics + beta blockers beta blockers + ccas ccas + acei acei + diuretics
isoproterenol
non selective beta agonist mainly used for bradycardia and heart block positive chronotropic, dromotropic and inotropic
sotalol
non selective b blocker that also exhibits class III antiarrhythims properties by inhibition of potassium channels used especially for ventricullar fib and VT
dobutamine
Beta 1 selective beta agonist used in tx of heart failure and cardiogenic shock increase CO NOT useful in ischemic heart dz because increases heart rate and increase myocardial o2 demand
