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drugs Flashcards

1
Q

<p class=”large” style=”text-align:center”;>propranolol</p>

A

<p class=”large” style=”text-align:center”;>non selective beta blocker
high lipid solubility
eliminated by liver</p>

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1
Q

<p class=”large” style=”text-align:center”;>atenolol</p>

A

<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>

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1
Q

<p class=”large” style=”text-align:center”;>what are class I and III antiarrhythmics used for</p>

A

<p class=”large” style=”text-align:center”;>vent tachy
atrial fib
AV reentry</p>

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1
Q

<p>carvedilol</p>

A

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>

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1
Q

<p>metoprolol</p>

A

beta 1 selective beta blocker
with moderate lipid solubility
eliminated by liver</p>

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1
Q

<p>atropine</p>

A

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>

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1
Q

<p>procainamide</p>

A

class Ia antiarrhythmic
tragets Ina and Ik
depresses fast response excitability and increases APD</p>

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1
Q

<p class=”large” style=”text-align:center”;>lidocaine</p>

A

<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>

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1
Q

<p>flecainide</p>

A 
class Ic antiarrhythmic
depress fast response excitability in noemal and depolarized tissue</p>
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1
Q

<p class=”large” style=”text-align:center”;>dofetilide</p>

A

<p class=”large” style=”text-align:center”;>class III antiarrhythmic
targets Ik
prolong APD without depressing excitability in fast response tissue</p>

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1
Q

<p>verapamil</p>

A

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>

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1
Q

<p>what are class I and III antiarrhythmics used for</p>

A

vent tachy
atrial fib
AV reentry</p>

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2
Q

<p class=”large” style=”text-align:center”;>factors that modify the strength of sodium channel blockade</p>

A

<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>

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2
Q

<p class=”large” style=”text-align:center”;>what are class IV antiarrhythmics, digoxin and adenosine used for</p>

A

<p class=”large” style=”text-align:center”;>AVNRT</p>

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2
Q

<p>what is unique about class Ia antiarrhythmic</p>

A

also blocks Ik so increased action potential duration</p>

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2
Q

<p class=”large” style=”text-align:center”;>factors that modify the strength of sodium channel blockade</p>

A

<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>

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3
Q

<p class=”large” style=”text-align:center”;>selectivity of calcium channel blockers</p>

A

<p class=”large” style=”text-align:center”;>verapamil - cardiac
nifedipine - vascular
diltiazem cardiac and vascular</p>

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3
Q

<p>factors that increase the effect of Ik blockade on APD</p>

A

slow hear rates
low extracellular K
low extracellular M</p>

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3
Q

<p>effect of digoxin in arrhythmia</p>

A

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>

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3
Q

<p>adenosine</p>

A

adenosine receptor agonist
decrease calcium current and icnrease potassium current from ach
onset of action and duration of effect is seconds!!</p>

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3
Q

<p class=”large” style=”text-align:center”;>what is major determinant of ERP in fast and slow response tissue?</p>

A

<p class=”large” style=”text-align:center”;>fast - APD
slow- recovery of ca channel</p>

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3
Q

<p class=”large” style=”text-align:center”;>selectivity of calcium channel blockers</p>

A

<p class=”large” style=”text-align:center”;>verapamil - cardiac
nifedipine - vascular
diltiazem cardiac and vascular</p>

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4
Q

<p class=”large” style=”text-align:center”;>prazosin</p>

A

<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>

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4
Q

<p class=”large” style=”text-align:center”;>how to tx afib</p>

A

<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>

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4
Q

<p class=”large” style=”text-align:center”;>conditions that raise risk of using antiarrhythmic drugs</p>

A

<p class=”large” style=”text-align:center”;>prolonged QT esp with low K, Mg
sick sinus node
AV block
poor systolic fx</p>

4
Q

<p class=”large” style=”text-align:center”;>prazosin</p>

A

<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>

5
Q

<p class=”large” style=”text-align:center”;>how are beta blockers used in CV medicine</p>

A

<p class=”large” style=”text-align:center”;>decrease HR, decrease impulse conduction, decrease cardiac contractility and metabolic rate

used in heart failure, MY/angina, arrhythmias, htn</p>

5
Q

<p class=”large” style=”text-align:center”;>alpha adrenergic antagonists</p>

A

<p class=”large” style=”text-align:center”;>prazosin, doxazosin, terazosin

zosin endings!
Doxa and tera are pura alpha 1 blockers
doxa and tera are slower onset and longer duration</p>

5
Q

<p class=”large” style=”text-align:center”;>beta adrenergic antagonists</p>

A

<p class=”large” style=”text-align:center”;>propranolol, metoprolol, atenolol, carvedilol

distinguished by beta 1 selectivity,
instrinsice sympathomimetic activity,
lipid solubility
duration of action

atenolol- hydrophilic- metabolized by kidney</p>

5
Q

<p class=”large” style=”text-align:center”;>ends for sympathetic antagonists & ace inhibitors</p>

A

<p class=”large” style=”text-align:center”;>beta antagonists - end with olol or ilol
alpha ends with zosin
ace inhibitor - pril</p>

5
Q

<p class=”large” style=”text-align:center”;>selectivity of beta blockers</p>

A

<p class=”large” style=”text-align:center”;>propranolol - beta 1 & 2 - nonselective
metoprolol & atenolol - beta 1 selective
carvedilol - non-selective with alpha 1 blockade!</p>

5
Q

<p class=”large” style=”text-align:center”;>how are beta blockers used in CV medicine</p>

A

<p class=”large” style=”text-align:center”;>decrease HR, decrease impulse conduction, decrease cardiac contractility and metabolic rate

used in heart failure, MY/angina, arrhythmias, htn</p>

6
Q

<p class=”large” style=”text-align:center”;>name ace inhibitors</p>

A

<p class=”large” style=”text-align:center”;>captopril
enalapril
lisinopril
rampipril</p>

6
Q

<p class=”large” style=”text-align:center”;>other enzymes that can make ang II</p>

A

<p class=”large” style=”text-align:center”;>CAGE
cathepsin G
chymase

from angiotensinogen –> angII
t-Pa
cathepsin G
tonin</p>

6
Q

<p class=”large” style=”text-align:center”;>arbs</p>

A

<p class=”large” style=”text-align:center”;>block AT1
downstream from alternative angII pathway
no build up of bradykinin (good & bad)
AT2 receptors still are able to be acivated</p>

6
Q

<p class=”large” style=”text-align:center”;>thiazide</p>

A

<p class=”large” style=”text-align:center”;>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)</p>

6
Q

<p class=”large” style=”text-align:center”;>two classes of calcium channel antagonists</p>

A

<p class=”large” style=”text-align:center”;>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</p>

6
Q

<p class=”large” style=”text-align:center”;>direct peripheral vasodilators</p>

A

<p class=”large” style=”text-align:center”;>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)</p>

6
Q

<p class=”large” style=”text-align:center”;>minoxidil</p>

A

<p class=”large” style=”text-align:center”;>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</p>

6
Q

<p class=”large” style=”text-align:center”;>beenfits of beta blockade in tx of ischemia</p>

A

<p class=”large” style=”text-align:center”;>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</p>

6
Q

<p class=”large” style=”text-align:center”;>losartan</p>

A

<p class=”large” style=”text-align:center”;>first synthetic antagonist to AT1 receptor</p>

6
Q

<p class=”large” style=”text-align:center”;>limitations of ace inhibitors</p>

A

<p class=”large” style=”text-align:center”;>non specific enzyme
alternate pathways for ang II
poor side effect profile - cough and rare angioedema</p>

6
Q

<p class=”large” style=”text-align:center”;>direct renin inhibitor</p>

A

<p class=”large” style=”text-align:center”;>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 - $$</p>

6
Q

<p class=”large” style=”text-align:center”;>toxicities of thiazide diuretics</p>

A

<p class=”large” style=”text-align:center”;>sulfa allergy
hypokalemia
promote insulin resistance
increase TG and LDL cholesterol</p>

6
Q

<p class=”large” style=”text-align:center”;>diltiazem</p>

A

<p class=”large” style=”text-align:center”;>non dihydropyridine CCA –> lowest incidence of SE and effective in tx SVT
not great htn drug</p>

6
Q

<p class=”large” style=”text-align:center”;>nifedipine</p>

A

<p class=”large” style=”text-align:center”;>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</p>

6
Q

<p class=”large” style=”text-align:center”;>hydralazine</p>

A

<p class=”large” style=”text-align:center”;>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</p>

6
Q

<p class=”large” style=”text-align:center”;>minoxidil</p>

A

<p class=”large” style=”text-align:center”;>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</p>

7
Q

<p class=”large” style=”text-align:center”;>mechanism of action of centrally acting alpha 2 adrenergic agonist</p>

A

<p class=”large” style=”text-align:center”;>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</p>

7
Q

<p class=”large” style=”text-align:center”;>tx of htn for isolated systolic htn</p>

A

<p class=”large” style=”text-align:center”;>diuretics reduce strokes</p>

7
Q

<p class=”large” style=”text-align:center”;>sodium nitroprusside</p>

A

<p class=”large” style=”text-align:center”;>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</p>

7
Q

<p class=”large” style=”text-align:center”;>reserpine</p>

A

<p class=”large” style=”text-align:center”;>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</p>

7
Q

<p class=”large” style=”text-align:center”;>centrally acting alpha 2 adrenergic agonist</p>

A

<p class=”large” style=”text-align:center”;>methyldopa
clonidine</p>

7
Q

<p class=”large” style=”text-align:center”;>tx of htn post mi</p>

A

<p class=”large” style=”text-align:center”;>Beta blocker
acei
Aldosterone agonist</p>

7
Q

<p class=”large” style=”text-align:center”;>tx of htn with dbm</p>

A

<p class=”large” style=”text-align:center”;>diuretic
aci
arb
cca</p>

7
Q

<p class=”large” style=”text-align:center”;>tx of htn for isolated systolic htn</p>

A

<p class=”large” style=”text-align:center”;>diuretics reduce strokes</p>

8
Q

<p class=”large” style=”text-align:center”;>amiodarone</p>

A

<p class=”large” style=”text-align:center”;>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</p>

8
Q

<p class=”large” style=”text-align:center”;>rational use of anti htn drugs in combo</p>

A

<p class=”large” style=”text-align:center”;>diuretics + beta blockers
beta blockers + ccas
ccas + acei
acei + diuretics</p>

8
Q

<p class=”large” style=”text-align:center”;>isoproterenol</p>

A

<p class=”large” style=”text-align:center”;>non selective beta agonist
mainly used for bradycardia and heart block
positive chronotropic, dromotropic and inotropic</p>

8
Q

<p class=”large” style=”text-align:center”;>sotalol</p>

A

<p class=”large” style=”text-align:center”;>non selective b blocker that also exhibits class III antiarrhythims properties by inhibition of potassium channels
used especially for ventricullar fib and VT</p>

8
Q

<p class=”large” style=”text-align:center”;>dobutamine</p>

A

<p class=”large” style=”text-align:center”;>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</p>

random cardio (6 decks)

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