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Year 2 CV > Exam 3 Linger CIS pharm > Flashcards

Exam 3 Linger CIS pharm Flashcards

1
Q

What are the cardio drugs WITHOUT positive ionotropic effects. can have negative

A 
diuretics
ACEI
ARB
vasodilators
beta adrenergic R blockers
Natriuretic peptide
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2
Q

which class of diuretics are the most efficacious for reducing volume overload?

A

loop diuretics

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3
Q

what are the loop diuretics

A

furosemide, bumetanide, tosemide, ethacrynic acid

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4
Q

how do loop diuretics work

A

inhibit luminal Na/K Cl cotransporter in TAL of Henle
dec intracell K, dec back diffusion of K.
dec reabsorption Ca and Mg. Inc diuresis

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5
Q

what are indications for furosemide and ethacyrnic acid

A

edema, heart failure, HTN, Acute renal failure, hypercalcemic states

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6
Q

prescribed furosemide and additional agent to control BP and edema
reaction is swollen tongue and nagging cough
what most likely caused it

A

ACEI “-pril”

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7
Q

why do ACEI cause cough and angioedema

A

blocks inactivation of bradykinin

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8
Q

which R do ARBs work on

A

AT1

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9
Q

CHF patient is stable on furosemide and losartan
thir drug is prescribed to improve survival in patients wit HF
Sx may initially get worse but dramatic improvement after 3-6 mo Therapy
which drug was most likley prescribed

A

beta blocker

like metoprolol

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10
Q

describe effects of high and low dose beta blockers

A

high can antagonize supportive effects of catecholamines and worsen HF

low can slow herat rate, increase Ejection fraction and decrease mortality

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11
Q

what are sprionolactone and plerenone

A

aldosterone antagonist

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12
Q

when are aldosterone antagonists used

A

on top of ACEI or ARB

not by itself

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13
Q

Patient develops palpitations and has presence of third Heart sound S3
has paroxysmal atrial tachycardia with block at toxic concentrations

A

digoxin

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14
Q

what type of drug is digoxin

A

cardiac glycosid

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15
Q

what are clinical indications for cardiac glycosides

A

heart failure, a fib and shock

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16
Q

how do cardiac glycosides work

A

inhibit membrane bound NaK ATPase and increase myocardial contractility

17
Q

does digoxin have effect on mortality

A

no

18
Q

how does digoxin effect Ca

A

increased intracell Ca so pumped into Sarcoplasmic Reticulum because cannot leave cell (concentration gradient gone from blocked Na/K ATPase

19
Q

Why does digoxin have many adverse effects

A

Na/KATPase in every part of body

main areas affected are GI and neuro

20
Q

how does digoxin change action potential

A

brief prolongation of action potential followed by shortening

21
Q

loking at action poetnetials of cardiomyocytes you see oscillatory depolarizing afterpotentnials following normally evoked action potentnials.
what drug toxicity could cause this

A

digoxin

22
Q

how does digoxin change sympathetic tone

A

therapeutic levels decreases sympathetics and increases parasympathetics
toxic levels increases sympathetics

23
Q

how does digoxin affect AV node at therapeutic doses

A

decreases conduction velocity and increases refractory period

24
Q

how does hyperkalemia effect figosxin

A

reduce the effects because hyperkalemia inhibitis abnomral cardiac automaticity

25
Q

which drug an potentiate toxic effects of digoxin

A

furosemide from hypokalemia and hypomagnesia

26
Q

what are the bipyridines

A

inamrinone and milrinone

27
Q

how do bipyridines work

A

prolong relaxation though do increase contractility

28
Q

when are bipyrdines worked

A

acute HF, very short term use

usually used in hospital setting

29
Q

how do bipyridines work

A

inhibit PDE3 which degrades cAMP

30
Q

which drugs increase mortality

A 
ACEI
ARBs
Beta blockers
aldosterone antagonists (after MI)
hydralazine with nitrate (african americans)

Year 2 CV (31 decks)

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