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cards long list Flashcards

1
Q

carvedilol

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

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2
Q

metoprolol

A

beta 1 selective beta blocker
with moderate lipid solubility
eliminated by liver

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3
Q

propranolol

A

non selective beta blocker
high lipid solubility
eliminated by liver

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4
Q

atenolol

A

beta 1 selective beta blocker
low lipid soluble
eliminated by kidney
longer action –> can be dosed once daily
class II antiarrhtyhmic

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5
Q

atropine

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

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6
Q

procainamide

A

class Ia antiarrhythmic
tragets Ina and Ik
depresses fast response excitability and increases APD

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7
Q

lidocaine

A

class Ib antiarrhythmic
Targets Ina
depresses fast response excitability especially in depolarized tissue
*not useful at normal resting potential

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8
Q

flecainide

A

class Ic antiarrhythmic
depress fast response excitability in noemal and depolarized tissue

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9
Q

dofetilide

A

class III antiarrhythmic
targets Ik
prolong APD without depressing excitability in fast response tissue

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10
Q

verapamil

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

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11
Q

what are class I and III antiarrhythmics used for

A

vent tachy
atrial fib
AV reentry

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12
Q

what are class IV antiarrhythmics, digoxin and adenosine used for

A

AVNRT

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13
Q

what is unique about class Ia antiarrhythmic

A

also blocks Ik so increased action potential duration

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14
Q

factors that modify the strength of sodium channel blockade

A

Ib< IA< IC
resting membrane potential - more potent when more negative
hear rate - more potent at faster heart rate

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15
Q

factors that increase the effect of Ik blockade on APD

A

slow hear rates
low extracellular K
low extracellular M

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16
Q

effect of digoxin in arrhythmia

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!

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17
Q

adenosine

A

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

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18
Q

what is major determinant of ERP in fast and slow response tissue?

A

fast - APD
slow- recovery of ca channel

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19
Q

selectivity of calcium channel blockers

A

verapamil - cardiac
nifedipine - vascular
diltiazem cardiac and vascular

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20
Q

how to tx afib

A

1) slow AV node -> atenolol, digoxin, verapamil
2) stop fibrillation in atrial muscle –> procainamide, amiodarone, sotalol, dofetilide, dlecainide

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21
Q

conditions that raise risk of using antiarrhythmic drugs

A

prolonged QT esp with low K, Mg
sick sinus node
AV block
poor systolic fx

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22
Q

prazosin

A

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

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23
Q

alpha adrenergic antagonists

A

prazosin, doxazosin, terazosin

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

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24
Q

beta adrenergic antagonists

A

propranolol, metoprolol, atenolol, carvedilol

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

atenolol- hydrophilic- metabolized by kidney

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25
Q

ends for sympathetic antagonists & ace inhibitors

A

beta antagonists - end with olol or ilol
alpha ends with zosin
ace inhibitor - pril

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26
Q

selectivity of beta blockers

A

propranolol - beta 1 & 2 - nonselective
metoprolol & atenolol - beta 1 selective
carvedilol - non-selective with alpha 1 blockade!

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27
Q

how are beta blockers used in CV medicine

A

decrease HR, decrease impulse conduction, decrease cardiac contractility and metabolic rate

used in heart failure, MY/angina, arrhythmias, htn

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28
Q

beenfits of beta blockade in tx of ischemia

A

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

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29
Q

losartan

A

first synthetic antagonist to AT1 receptor
potentially used to correct aortic phenotype of marfans syndrome
improves aortic dilatation in severely affect children

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30
Q

name ace inhibitors

A

captopril
enalapril
lisinopril
rampipril

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31
Q

limitations of ace inhibitors

A

non specific enzyme
alternate pathways for ang II
poor side effect profile - cough and rare angioedema

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32
Q

other enzymes that can make ang II

A

CAGE
cathepsin G
chymase

from angiotensinogen –> angII
t-Pa
cathepsin G
tonin

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33
Q

arbs

A

block AT1
downstream from alternative angII pathway
no build up of bradykinin (good & bad)
AT2 receptors still are able to be acivated

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34
Q

direct renin inhibitor

A

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 - $$

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35
Q

thiazide

A

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)

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36
Q

toxicities of thiazide diuretics

A

sulfa allergy
hypokalemia
promote insulin resistance
increase TG and LDL cholesterol

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37
Q

two classes of calcium channel antagonists

A

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

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38
Q

diltiazem

A

non dihydropyridine CCA –> lowest incidence of SE and effective in tx SVT
not great htn drug

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39
Q

nifedipine

A

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

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40
Q

direct peripheral vasodilators

A

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)

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41
Q

hydralazine

A

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

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42
Q

minoxidil

A

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

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43
Q

sodium nitroprusside

A

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

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44
Q

mechanism of action of centrally acting alpha 2 adrenergic agonist

A

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

45
Q

reserpine

A

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

46
Q

centrally acting alpha 2 adrenergic agonist

A

methyldopa
clonidine

47
Q

tx of htn post mi

A

Beta blocker
acei
Aldosterone agonist

48
Q

tx of htn with dbm

A

diuretic
aci
arb
cca

49
Q

tx of htn for isolated systolic htn

A

diuretics reduce strokes

50
Q

rational use of anti htn drugs in combo

A

diuretics + beta blockers
beta blockers + ccas
ccas + acei
acei + diuretics

51
Q

isoproterenol

A

non selective beta agonist
mainly used for bradycardia and heart block
positive chronotropic, dromotropic and inotropic

52
Q

sotalol

A

non selective b blocker that also exhibits class III antiarrhythims properties by inhibition of potassium channels
used especially for ventricullar fib and VT

53
Q

amiodarone

A

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

54
Q

dobutamine

A

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

55
Q

statins

A

tx high cholesterol by inhibting hmg coa-reductase (rate limiting step in cholesterol synthesis)
since pool of cholesterol reduced in liver - upregulates ldl receptors and reduces plasma ldl
se: increased liver transaminase
muscle side effects

56
Q

ezetimibe

A

cholesterol absorption inhibitor
inhibits absorption by binding and inhibting cholesterol transport NPC1L1
reduces hepatic cholesterol stores –> upregulation of LDL receptor

reduces LCL by 18-20%
not yet shown to reduce CV events
usually well tolerated - elevated transaminases

57
Q

bile acid sequestrants (BAS)

A

large insoluble anion-exchange resins that bidn bile acids in the intestinal lumen and prevent their re-absoprtion

cholestyramine, colestipol, colesevelam
not absorbed when given orally

reduced LDL by 15 - 25%, can raise TG levles
can result in constipaton, bloating, flatulance, heartburn nausea

58
Q

new approach to reducing LDL and CHD

A

inhibition of Pcsk9 –> usually targets LDL receptor for degeneration

59
Q

mipomersen

A

is a cholesterol-reducing drug candidate. It is an antisense therapeutic that targets the messenger RNA for apolipoprotein B.
It is administered as a weekly injection.

60
Q

lomitapide

A

treatment of familial hypercholesterolemia
inhibits the microsomal triglyceride transfer protein (MTP or MTTP) which is necessary for very low-density lipoprotein (VLDL) assembly and secretion in the liver

61
Q

fenofibrate

A

fibric acid derivative
activate the nuclear receptor PPARalpha in liver and peripheral tissues to affect multiple aspects of lipid metab

increase HDL production
decrease VLDL production
increase VLDL clearance
decrease LDL particles and increased size

62
Q

efficacy of fibrates

A

decrease TG levels by 20 - 50%
increase HDL 5 - 20%
mixed CV outcomes

used for severe hypertriglyceridemia (TG>500) to prevent pancreatitis

63
Q

anti-atherogenic HDL functions

A

antioxidant
antiinflammatory
antithrombotic
NO-promoting
cholesterol eflux and reverse chol transport

64
Q

omega 3 FA

A

EPA & DHA
in pts with hypertriglyceridemia, descrease TG levels by 30-50% and raise HDL levels modestly (105)
OTC and no outcome data

65
Q

nicotinic acid/niacin

A

hypolipidemic agent at high dosage –> reduces FFA release and flux to liver (antilipolysis)
decreases VLDL production

66
Q

efficacy of niacin

A

increase HDL 20-30%
dec TG levels 20-40%
dec LDL 15-35%
decrease LP(a) by 15-30%

not effective in reducing CVD
flushing report in 88% of pts
no longer used

67
Q

endrophonium

A

parasympathetic agonist –>ACH esterase inhibitor
stimulates strong parasympathetic discharge
also profound abdominal cramping bc stimulates GI muscles
*used for - AV nodal refractoriness for brief periods (ie diagnosing supraventricular tachy due to AVNRT or AV bypass tract –> in clinical use surpassed by adenosine that does same thing without GI SE

68
Q

parasympathetic agoniest

A

atropine, acopolamine

69
Q

sympathetic agonist

A

E, NE, pheylephrine, isoproterenol, dobutamine, dopamine

70
Q

sympathetic antagonist

A

prazosin, carvedilol, atenolo, metoprolol, propanolol

71
Q

epinephrine

A

mized alpha, beta 1 & 2 agonist

used most commonly in cardiopulm bypass or resusucitations
can cause platelet aggregation –> DON_T USE IN MI

72
Q

norepinephrine

A

mixed alpha 1 & neta 1 agonist (little b2)

powerful vasoconstrictor but only modesly inotrope

73
Q

dopamine

A

mixed a/ba (little b2)
isolated d1 at low doses
very short half life

74
Q

dopamine dose effects

A

low dose –> renal vasodilation
intermediate dose –> b1 plus d1 –> increase CO with mininal effect on SVR (inhibits reuptake of NE indirect beta stimuation)
high dsoe –> alph action overwhelms d1 action –> effect similar to NE

renal
inotrope
pressor

*infiltation of IV site can lead to necrosis of skin

75
Q

phenylephrine

A

predominant alpha agonist with little beta activity

76
Q

isoproterenol

A

b1 + b2 activity with little alpha acitivity

pwerful chronotropic effect –> usef exclusively after heart transplant to drive HR and decrease PVR

77
Q

dobutamine

A

predominant b1 activity
mostly inotopic with little chronotropic activity
considered pure inotrop with modest effect on HR
effective for circulatory support in severe CHF
chronic infusion –> desensitization
short acting–> plasma half life is 2 minutes

used to pharmacologically stimulate exercise

78
Q

inotropic mechanisms

A

B receptor stimulation –> increase cAMP –> PKA activation –> phosphoryation of phosopholamban –> increase Ca uptake into SR so greater release

PDE3 inhibitors–> decrease cAMP hydrolysis

digitalis –> inhibits Na/K exhanger which then decrease Ca intake via Na/Ca exchanger

79
Q

digoxin

A

competitivly inhibits Na-KATPase (low K+ is dangerous)
*no desensitization or tolerance
*increases intracellular Ca cause increase inotropy without inc HR

80
Q

dig pharmokinetics

A

half life 36 hours
renal clearance
therpaeutic level - .5 to 1.0

81
Q

effects of dig

A

1) hemodynamic –> inc CO, inc LVEF, dec LVEDP, Inc exercise tolerance, inc natriureis

2) neurohormonal –> dec plasma NE, dec PNS activity, dec RAAS acitivity, increase vagal tone

3) electrophys prop –> atrial and vent muscles and specialized cardiac pacemaker and conduction fibers exhibit differeing responses and sensitivities to dig

*be careful wtih drug drug interactions - very common

82
Q

stange impact of dig on conduction

A

increae vagal tone and dec sympathetic activity
abnormal automaticity and direct increase in RP of AV node in toxic levels –> increased risk brady/heart block
slow response tissues can get blocked and fast response can become even more excitable
ventricular effects–> increase automaticity, delayed after depolarizations leading to increased risk fo vtech and vfib

83
Q

dig clinical uses

A

afib with rapid ventricular response
CHF symptoms despite medical tx
(be careful in use with bb –> heat block)
goal to .5 to 1.0

84
Q

PDE3 inhibitors

A

increase contractility via increase in Ca WITHOUT increase HR
potent vasodilators including venous capacitance vessles and pulm vasc bed

85
Q

uses of PDE3 inhibitors

A

decompensated HF
-improve systolic and diastolic fx
improve exercise tolerance
venodilator and pulm vasodilator
inhibits platelt aggregation

86
Q

warnings about pde3

A

**Significant hypotension can occur if filling pressures are not elevated (bc venodilator properties of PDE inhibitors drop pre load and afterload at same time)
**need to know pt is volume overloaded

87
Q

PDE3 inhibitors

A

amrinone
milrinone–> only one currently used - long half life of 2,3 hours, renal elimintaion

88
Q

acute care of ACS

A

1) anti-ischemic tx –> nitroglycerin (NTG), b-blcoker, CCB
2) antithrombotics - antiplatelets: aspirin, thienopyridine, glycoproteinIIb, IIIa receptor inhibito
anticoag: heparin, direct thrombin inhitiors, factor Xa inhibitors
3) reperfusion: PCI, CABG

89
Q

direct thrombin inhibitors

A

used in ACS

bivalirudin
dabigatran

90
Q

antithrombotics used in ACS

A

UFH
heparin
bivalirudin
dabigatran

91
Q

factor Xa inhibitors

A

UFH
LMWH
fondaparinux

92
Q

P2Y12 inhibitors/ADP

A

clopidogrel
prasugrel
ticagrelor

93
Q

gpIIb-IIIA inibitors

A

abciximab (ReoPro)
eptifibatide (Integrilin)
tirofiban (Aggrastat)

94
Q

acute care of STEMI

A

1) anti-ischemic tx –> nitroglycerin, Beta blockers
2) anti-thrombotics - antiplatelets, anticaog
3) reperfusin –> fibinolytics, PCI, CABG

  • time is muscle -> early and rapid reperfusion
95
Q

what can cause angina

A

CAD
valvular heart dz
hypertrophic cardiomyopathy

96
Q

how to tx patient with stable angina

A

aspirin
beta block –> great antianginal med
acei or arb
statin

97
Q

thienopyridine

A

ADP/P2Y12 inhibitor
used in pts who have MI or intracoronary stents placed –> in combo w aspirin
increased risk fo bleeding over aspirin

98
Q

echocardiogram

A

can assess LVEF and regional wal lmotion abnormalities

99
Q

exercise stress test with nuclear perfusion imaging

A

looks for evidence of ischemia

100
Q

exercise stress test with echo

A

reproduces pt symptoms and look for evidence of ischemia by seeing wall motion abnormality (one of earliest signs of myocardial ischemia) and alert physician to extent and severity of ischemia and help guide tx

101
Q

cardiac cathetierization and coronary angiography

A

test is gold standard in dx of CAD
invasice but safe and offers possibility fo angioplasty and intracoronary stenting

102
Q

tx of unstable angina

A

aspirin
heparin (interferes with thrombus formation at different site than aspirin)
thienopyridine (if not undrgoing early angiography and revasculuarization)
GPIIb/IIIa inhibitor - only IF pt IS undergoing PCI

103
Q

what meds to give pt with STEMI who is heading to cath lab

A

apirin
IV heparin infusion
clopidogrel

104
Q

nuclear med - strengths, limitations, clinical use

A

strength: noninvasice CAD diagnosis
excellent prognostic capability

limit: use ionizing radiation
moderately accurate
cost

use: CAD, myocardial viability

105
Q

coronary angiography

A

strength: accuracy in CAD dx
limit: lumenogam, invasiv study, contract agent required, uses ionizing radiation

use: CAD

106
Q

echocardiogram - +/- uses

A

strengths - portable, noninvasic, delineates structure and function
limit - imagine quality not ideal in ALL cases, TEE smi-invasice, less infor re: coronary artery stenoses
use: structural HD, coronary artery dz (wall motion)

107
Q

cardiovascular CT

A

strength- less invasive than CA,visualizes coronary wall, excellent for aortic and peripheral dz
limit- less accruate than CA, contrast agent required, uses ionizing radiation
uses - vasculary and coronary artery dz

108
Q

cardiac mri

A

strength- excellent delineartion of structure and function, noninvasive, visualizes coronary wall

limit- not as widely available, not portable, cost
use - structural heart dz, CAD - perfusion, myocardial viability

random cardio (6 decks)

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