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drugs from book Flashcards

1
Q

categories of inotropic drugs & how they work

A

cardiac glycosides
sympatheomimetic amines
PDE3 inhibitors

all enhance cardiac contraction by increasing intracellular calcium concentration
shift frank-starling curveupward - so fof given Ven filling pressure –> SV & CO increased

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2
Q

two desired effects of digitoxin

A

1) improve contractility of failing heart
2) prolong refractorey period of the AV node in pts with SV arrhythmias

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3
Q

MOA of digoxin/digitalis

A

1) mechanical effect:
inhibition of sarcolemmmal Na/K aTPase pump
increase intracellular Na –> decreases amount of Ca extruded via Na/Ca exchanger–> so more Ca is pumped into SR
-subsequent AP more ca is released –> enhances force of contraction

2) electrical effect –> slows conduction velocity & increases refractoriness at AV node
modifies autonomic nervous system by enhancing vagal tone and reducing sympathetic activity

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4
Q

dangers of digitoxin

A

1) less negative resting potential –> bc inhibition of N/K atpase –> partial inactivation of fast Na channels - slower rise of phase 0 depolarization & reduction in conduction velocity –> can increase risk for reentrant arrhthmias
2) decreased action potential duration –> at high concentrations of dig –> elevated intracellular calcium increased acitvity of CA dependent K_ channel –> opening of thi schannel promotes K+ efflux and more rapid repolarization (also higher intracel Ca inactivates that Ca channels decreasing inward depolarizing curent) –> descrease in AP duration and associated shoretened refractory period increase the time during which cardiac fibers are responsive to external stimulation –> opportunity for propogation of arrhythmic impulses
3) enhanced automaticity –> less neg resting potential (may induce phase 4 depolairzation in nonpacemaker cells) & dig induced increase in Ca may trigger delayed afterpolarizations

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5
Q

clinical uses of digoxin

A

1) historically used to tx HF caused by decreased vent contracility ** only useful in HF if contactility failing
now usef in pts with HF complicated by afib or when symptoms don’t respond to acei, bb and diuretics
*does not prolong life expectancy of pts with CHF but improves QOL

2) antiarrhythmic agent in afib, a flutter and PSVT
(less common bc BB, CCB and amiodarone are more effective)

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6
Q

risk factors for dig toxicity

A

–> further inibits pump
hypomagnesemia
hypercalcemia

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7
Q

sympathomimetic amines MOA

A

bind cardiac Beta1 receptors –> increase acitivty of adenyalte cyclase, –> increased formation of cAMP
-increase cAMP activates protein kinases which promote intracellular Ca influx by phosphorylating L-type calcium channels –> increase calcium tentry triggers corresponding increase in Ca release from SR –> enhances force of contraction

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8
Q

names of sympathomimetic amines

A

dopamine & dobutamine –> used for acute HF (IV)
norepinephrine, epineprhine & isoproterenol

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9
Q

dopamine - clincial uses

A

precursor to norepi
1) low doses–> dopaminegic receptors in renal and mesenteric vascular beds –> local vasodilation & increases renal blood flow and glomerular filtarion, facilitating diuresis
2) medium doses –> increase inotropy by stimulating B1 receptors directly and indirectly promoting release of norepi from sympathetic nerve terminals
3) high doses –> dopa also stimulates alpha receptors –> vasocontriction and elevating systemic resistance –> high dose dopa in hypotensive states such as shock
loses efficacy after one week bc downregulation of receptors

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10
Q

dobutamine

A

synthetic dopamine that stimulats B1,2 &alpha
increase cardiac contractility (b1) but does nto increae peripheral vascular reistance bc balance bw alpha mediated vasocon and b2 mediated vasodil
useful in tx of HF not accompanied by hypotension
loses efficacy after one week bc downregulation of receptors

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11
Q

norepinephrine

A

B1 and alpha activity
B1 –> +inotropinc and chronotropic effects
potent vasocon
useful in pts with warm shock –> bc they have cardiac contactile dysfx and peripheral vasodilation (low BP)

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12
Q

epinephrine

A

alpha, b1 & b2
IV in low doses –> mostly b1 –> increases vent contractilty and speeds impulse generation & b2 –> vasodil reduct TPV and BP
higher doses –> potent vasopressor bc alpha action dominates b2

used most often in cadiac arrest –> combo of inotropic and chronotropic and vasoconstriction also helps in this setting
**not used w beta blockers –> bc unopposed alpha activity –> raise arterial bp

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13
Q

isoproterenol

A

synthetic epi but PURE beta - beta 1 & 2
+ inotropic and chronotropic effects –> increases CO
peripheral vasodilation –> reduction in peripheral resistance

used in emergenceis to increase heart rate in pts with brady or heart block
*not used in pts with my ocardial ischemia

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14
Q

milrinone

A

PDE 3 inhibitor –> inotropic agent
inhibition reduces breakdown of cAMP –> leads to enhanced Ca entry into cell and increaed contraction
in VSM –> increase cAMP results in vasodilation (b/c cAP inhibits myosin light chain kinases)
used to tx acute heart failyre when conventional vasocilators, inotropic agents and diuretics havent worked
potential for serious SE–> only used in hospital in ST

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15
Q

vasopressin

A

natural vasodilator that regulates water
at higher-than-natural doses potent vasoconstrictor bc directly stimulates vascular smooth muscle –> maintains BP for patients in vasodilatory shock

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16
Q

why is vasoconstriction initally helpful in HF?

A

maximaizes LV preload (increases venous tone enhances venous return) and helps to maintain systemic BP (bc of arterial constriction)

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17
Q

vasodilator drugs (names)

A

venodilators –> nitrates
mixed –> nitroprusside, aci, arbs, alpha blockers alpha 2 central agonist, nesiritide
arteriolar dilators–> hydralaizine, minoxidil, ccb

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18
Q

effects of acei

A

decreases systemic arterial pressue, facilitate natriursis, reduce adverse ventricular remodeling
increase BK (bc ace normally breaksdown) –> contributes to antihypertensive effect by stimulating release of NO

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19
Q

clincal uses of acei

A

1) htn –> descrease BP with little change in CO or HR (similar effect to BB & diuretics WITHOUT adversely affecting serum glucose or lipic concentrations so used in diabetic htn bc may slow diabetic nephropathy development
2) HF–> reduces afterload (PVR), reduce cardiac filling pressure (preload) and increase CO (BP unchanged due to balance) –> augmented CO lowers sympathetic stimulation –> so less norepi
improve survival in CHF and following MI

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20
Q

arbs

A

1)compete with angII at AT1 receptors –> more complete block of angII than acei bc alternative pathways
but do not affect BK levels
as effective as acei and are better tolerated
as with acei - htn effect is enhance with concurrent use of thiazide diuretic

2) severt HF - hemodynamic effects similar to acei (used in hf for pts intolerant of acei)

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21
Q

direct acting vasodilators - names

A

hydralazine
minoxidil
soidum nitroprusside
fenoldopam

first two used as LT oral agents
seoncd two IV in acute setting

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22
Q

hydralazine

A

potent and direct arteriolar dilator that acts on precapillary arterioles & no effect on systemic veins
MOA-unknown

fall in BP–> sympathetic activation –> tachy so often given with bblocker
not used often for htn
used to tx hf in pts with systolic dysfx with venodilatoer dinitrate –> improves symtpoms in pts with mild to moderate hf

**acetylated for excretion in liver –> varying degree of acetlyators!
SE- headache, palpitations, flushing, nauseua, anorexia

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23
Q

minoxidil

A

arteriolar vasodilatorion without venous impact
increase K channel permeability –> smooth muscle hyperpolarization and relaxation
often coadministered with BB

used for severe or intractable htn

SE-fluid retention & hypertrichosis

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24
Q

soidum nitroprusside

A

potent dilator of arteries and veins
IV for hypertensive emergencies & for preload and afterload modulation in severe CHF

metabolized by rbc –> liberates NO–> activates guanylate cyclase in VSM
Bblocker concurrently
onset within 30 seconds & peak with in 2 minutes

metabolized into cyanide –> liver transofrms into thiocyanate (levels msut be monitored)

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25
Q

effect of CCB in VSM

A

contraction of VSM depends on cytoplasmic ca concentration –> CCBs promote relaxation of VSM by inhibiting Ca entry thorugh voltage gated channels

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26
Q

effect of CCB in cardiac muscle

A

interfere with excitation contraction coupling and decrease force of contraction
also will slow rate of SA and AV firing if binds to open channel (verapamil & diltiazem)

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27
Q

CCB clinical uses

A

1) angina pectoris –> decrease myocardial o2 comsumption & increae supply (dilation)
2) coronary artery spams –> vasodilate
3) htn –> arterial smooth muscle relazation
4) SV arrthymias –> decrease conduction velocity & increase refrcatoriness of AV node

**often used in htn –> more than bb and aci espeically in elderly pts

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28
Q

organic nitrates (nitroglycerin)

A

produce vsm relaxation –> drug converted to NO which activates guanylate cyclase to product cGMP –> increase intracellular cGMP leads to SM relaxation

29
Q

clinical use of nitroglycerin

A

primary to tx angina pectoris –> venodilation leading to reduced LV preload –> smaller V size lowers venti wall stress and myocardial o2 consumption
alleviates o2 imbalance

30
Q

nesiritide

A

human recombinant b type natriuretic peptide –> promote vasodilation and result in sodium and water excretion,
augments CO
not really used clinically –> doesn_t improve survival in HF

31
Q

central adrenergic inhibitors (alpha 2 agonist)

A

alpha 2 receptors in presynaptic neurons oc CNS –> when stimualted by alpha 2 agonist –> diminished sympathetic outflow from medulla
reduces PVR and dec cardiac stimulation –> dec bp and hr
used to be used commonly as anti htn

clonidine can be used as skin patch - 1 week

SE dry mouth, brady, sedation

32
Q

reserpine

A

inhibitsuptake of norepi into storage vesicles in postgan and central neurons –> norepi degradation
depletion of catecholamines –> dec mycoardial cont and total peripheral resistance

SE cns toxicity - depression = not used

33
Q

alpha 1 receptor selective antagonists & use

A

prazosin, terazosin, doxazosin
had been used for htn btu more adverse events than diuretics so not used as often
now mostly used to tx symptoms of benign prostatic hyperplasia

34
Q

nonselective beta antagonist

A

carvedilol - also alpha
labetalol - also alpha
propranolo
nadolo
timolol

35
Q

beta 1 selective antagonists

A

atenolol
metopolol

36
Q

uses for bb

A

1) ischemic heart dz –> dec o2 demand & increase survival post mi
2) htn –> lt effect not really known
3) HF –> clinically stable hf –> may blunt cardiotoxicity of circulationg catecholamines
4) tachy arrhythmias

37
Q

adverse effects of bb

A

1) bronchospasm
2) impair AV node conduction by b1
3) b2 can worsen raynaud (arterial vasospasm)
4) cant withdraw abruptly
5) reduce HDL
6) can mask hypoglycemia in diabetics

38
Q

classes of antiarrhythmics

A
  1. Class I drugs block the fast sodium channel
    responsible for phase 0 depolarization of the
    action potential. They are further divided into
    three subtypes based on the degree of sodium
    channel blockade and the effect of the drug
    on the cell_s action potential duration.
  2. Class II drugs are -adrenergic receptor antagonists
    ( -blockers).
  3. Class III drugs block potassium channels
    responsible for repolarization, thereby prolonging
    the action potential with little effect
    on the rise of phase 0 depolarization.
  4. Class IV drugs block the L-type calcium
    channel.
39
Q

tx aims for arrythymia by increased automaticity

A

1) reduce slope of spontaenous depolarization of phase 4
2) prolong ERP

40
Q

aims to stop reentry circuits

A

1) prolong ERP
2) impair impulse propagation wthin already slowed retrograde limb –> blockade of Na channels responisble for phase 0

41
Q

aim to stop triggered arrhythmia

A

supression of early and dealyed after depolarizations

42
Q

class IA uses

A

1) reentrant arrhythmia –>
2) ectopic supraventricular tachy
3) vent tachy

procainamide

43
Q

class I B uses

A

inhibit the fast Na channel but SHORTEN AP (unlike class I)
only work on depolarized cell –> target damaged cells

1) Vent arrhythmias esp those associated with ischemia or dig tox
little effect on atrial tissue (bc of shorter AP of atrial tissues)

lidocaine - IV administration only

44
Q

class IC uses

A

most potent Na channel blockers
markedly decrease upstroke of AP and conduction velocity in atrial, ventricular and purkinje fibers
prolong AV ERP (but not elsewhere)

tx supraventricular arrhythmias
flecainide

45
Q

use of class II

A

used in both supravent and vent arrhythmias
slow vent rate in atrial flutter and fib by impairing conduction and increasing refractoriness of AV node

inhibit beta adeneregic effect of more rapid upslope of phase 4 depolarization & increased firing of SA node (reduce automaticity) & ltos more

46
Q

amiodarone

A

major therapeutic effect is to prolong AP duraction and refractoriness of all cardiac regions
-dpresses phase 0 depolarization slope through Na channel blockade
-b blocking effect and weak ccb

-dec SN diring rate, suppress automaticity, interrupt reentrant circuits and prolong PR, QRS, QT intervals

also vasodilator and negative inotrope

47
Q

uses of amiodarone

A

1) afib
2)a flutter
3) vent tachy
3) vent flutter
5) SVT including bypass tracts

48
Q

sotalol

A

nonselective b beta bocker but also oral antiarrh drug bc additional class III properties –> prolongs AP duration, increase RP of atrial and vent tissues and inhibits conduction in accessory bypass tracts
tx both SV and V arrh

49
Q

class IV

A

verapamil & diltiazem –> impact SA and AV nodes
-dec rate of rise of phase 0 depol and conduction velocity and lengthens RP of AV node

50
Q

use of class IV

A

primary used for tx of reentrant SVT (eg AVNRT)

51
Q

adenosine

A

most effective drug for rapid termination fo reentrant SVT (eg AVNRT)
binds adenosine receptors –> activates K channels –> hyperpolarizes membrance –> suppresses spontaneous depol of SA node and slows conduction through AV node
-decreases intracellular cAMP –> decrease in inward pacemaker current (If) and inward calcium current)
10 second half life

52
Q

statins

A

inhibit hmg coA reductase - most effective drugs for reducing LDL cholesterol
rate controlling step in cholesterol synthesis
lower cholesterol by reducing pool so more LDLR –> more taken out of blood
reduce serum LDL by 20-55% & decrease plasma TG by 7-30% & HDL increase 5-15%

53
Q

bile acid sequestrants

A

cholestyramine, colestipol & colesevelam

bind bile acids in intestine and prevent reabsorption –> to make up for loss more hepatic cholesterol is converted into newly produced bile acids
dec pool –> increase LDLR but since increase in VLDL production –> elevated TG

54
Q

cholesteroal absorption ihibitors

A

ezetimibe –> competitively inhibits transport NPC1L1 –> reduced chylomicron production —> increase LDLR on liver to make pool bigger

55
Q

niacin

A

raises HDL cholesterol and reduced LDL and TG, reduces LPL(a)
inhibits lipolysis –> less FA into liver and less VLDL also enhances LPL at adipose and muscle cells
*flushing as side effects

56
Q

fibrates

A

gemfibrozil and fenofibrate –> reduce TG by 50% and raise HDL by 20% but LDL effect variable
acton PPAR alpha –> dec TG by augmenting FA ox, increased VLDL cata b–> inc LDL :( –> actviate gene for apoprotein A1–> increase HDL

57
Q

tx to prevent recurrent ischemic episodes

A

BB -> decrease recurrent MI and mortality following acute MI
organic nitrates –> purely symptomatic relief no improval in survival
CCB

58
Q

clopidogreal

A

novel antiplatelet agent that blocks platetely P2y12 receptor –> preventing platelet activation and aggregation
can be used in pts allergic to aspirin or in combo with aspirin

59
Q

two types of diuretic

A

thiazide - HCTZ

Loop - furosemide

60
Q

non selective alpha inhibitor

A

phenoxybenzamine

61
Q

selective alpha blocker

A

prazosin

62
Q

central alpha blcoker

A

clonidine

63
Q

aldosterone antagonist

A

spironolactone

64
Q

arterial vasodilators

A 
hydralazine
sodium nitroprusside (IV drip)
65
Q

venodilators

A

nitrates

66
Q

Inotrope Pressor Vasoactive drugs

A

a. Epinephrine
b. Norepinephrine
c. Dopamine
d. Dobutamine
e. Isoproterenol
f. Phenylephrine
g. Milrinone

67
Q

Acetylcholinesterase inhibitors

A

edrophonium, physostigmine, neostigmine

68
Q

Class I (Na channel blockers)

A

a. Ia Procainamide/Quinidine
b. Ib Lidocaine
c. Ic Flecainide

69
Q

Class III (K channel)

A

Amiodarone, Sotalol

random cardio (6 decks)

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