Exam 3 Linger CIS pharm Flashcards
What are the cardio drugs WITHOUT positive ionotropic effects. can have negative
diuretics ACEI ARB vasodilators beta adrenergic R blockers Natriuretic peptide
which class of diuretics are the most efficacious for reducing volume overload?
loop diuretics
what are the loop diuretics
furosemide, bumetanide, tosemide, ethacrynic acid
how do loop diuretics work
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
what are indications for furosemide and ethacyrnic acid
edema, heart failure, HTN, Acute renal failure, hypercalcemic states
prescribed furosemide and additional agent to control BP and edema
reaction is swollen tongue and nagging cough
what most likely caused it
ACEI “-pril”
why do ACEI cause cough and angioedema
blocks inactivation of bradykinin
which R do ARBs work on
AT1
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
beta blocker
like metoprolol
describe effects of high and low dose beta blockers
high can antagonize supportive effects of catecholamines and worsen HF
low can slow herat rate, increase Ejection fraction and decrease mortality
what are sprionolactone and plerenone
aldosterone antagonist
when are aldosterone antagonists used
on top of ACEI or ARB
not by itself
Patient develops palpitations and has presence of third Heart sound S3
has paroxysmal atrial tachycardia with block at toxic concentrations
digoxin
what type of drug is digoxin
cardiac glycosid
what are clinical indications for cardiac glycosides
heart failure, a fib and shock
how do cardiac glycosides work
inhibit membrane bound NaK ATPase and increase myocardial contractility
does digoxin have effect on mortality
no
how does digoxin effect Ca
increased intracell Ca so pumped into Sarcoplasmic Reticulum because cannot leave cell (concentration gradient gone from blocked Na/K ATPase
Why does digoxin have many adverse effects
Na/KATPase in every part of body
main areas affected are GI and neuro
how does digoxin change action potential
brief prolongation of action potential followed by shortening
loking at action poetnetials of cardiomyocytes you see oscillatory depolarizing afterpotentnials following normally evoked action potentnials.
what drug toxicity could cause this
digoxin
how does digoxin change sympathetic tone
therapeutic levels decreases sympathetics and increases parasympathetics
toxic levels increases sympathetics
how does digoxin affect AV node at therapeutic doses
decreases conduction velocity and increases refractory period
how does hyperkalemia effect figosxin
reduce the effects because hyperkalemia inhibitis abnomral cardiac automaticity
