Cardiac Pharmacology

Front 1

effect of inotropic drugs

Back 1

increased force of contraction

Front 2

examples of inotropic medications

Back 2

glycosides (digitalis), da, dobutamine, norE, epi, PDE inhibitors (milrinone)

Front 3

moa of digitalis

Back 3

inhibits the na-k pump in the cardiac myocyte, which then causes the na/ca exchanger to allow more ca into the myocyte --> sr --> increased contractile force

Front 4

effects of digitalis on heart

Back 4

decreases conduction through av node (useful in svt), increased contractility (useful in chf)

Front 5

clinical uses of digitalis

Back 5

pt with chf + afib
of chf refractory to ace-i, diuretics, and bb
anti-arrhythmic for a-fib, a-flutter, psvt, but not as useful as bb, ccb, adenosine

Front 6

sx of dig toxicity

Back 6

life threatening arrhythmias

Front 7

tx of dig toxicity

Back 7

temp pacemaker
Fab of anti-dig fragments
lidocaine

Front 8

what is da a precursor to

Back 8

norE

Front 9

what receptors does da affect

Back 9

at low doses: d1 (--> increased renal perfusion and diuresis)
int. doses: b1 >b2
high doses: a1, b

Front 10

how does da affect the beta receptors

Back 10

directly stimulates receptors and also --> increase of norE release

Front 11

indications for da

Back 11

shock (increases svr)

Front 12

side effects of da

Back 12

increased hr --> increased o2 consumption, tachyarrhythmias

Front 13

receptors affected by dobutamine

Back 13

b1, b2, alpha agonist

Front 14

effects of dobutamine of svr

Back 14

none, b/c alpha and b2 effects counteract each other

Front 15

uses for dobutamine

Back 15

chf s low bp

Front 16

receptors affected by norE

Back 16

b1, alpha agonist (NO B2 EFFECTS!)

Front 17

effects of norE

Back 17

potent vasoconstriction (unopposed a stimulation)
increased hr and contractility

Front 18

uses of norE

Back 18

warm shock,

Front 19

receptors affected by epi

Back 19

a1, b1, b2 agonist
in low doses: b1, b2 (increased sv, hr, co, and vasodilation)
at high doses, a > b2 (potent pressor)

Front 20

uses of epi

Back 20

cardiac arrest

Front 21

side effects of epi

Back 21

tachyarrhythmias

Front 22

who should not receive epi

Back 22

pts with bb, b/c unopposed a mediated vasoconstriction --> very very high bp

Front 23

moa of pde inhibitors

Back 23

decreased breakdown of camp --> increased ca entry into cells --> increased contractile fore
also --> vasodilation

Front 24

exmples of pde inhibitors used in cardiology

Back 24

milrinone
amrinone

Front 25

uses for pde inhibitors

Back 25

chf if conventional vasodilation, dig, and diuretics don't work

Front 26

side effects of epi

Back 26

tachyarrhythmias

Front 27

physiology behind why there is vasoconstriction in chf

Back 27

decreased co --> increased adrenergic stimulation and raas activation --> vasoconstriction

Front 28

downside of physiologic vasoconstriction in chf

Back 28

initially it is beneficial b/c there is increased preload b/c of venous constriction and bp is also maintained.
eventually, venous constriction --> too much vr --> increased pulmonary capillary pressure --> pulmonary edema
therefore, tx is vasodilation

Front 29

who should not receive epi

Back 29

pts with bb, b/c unopposed a mediated vasoconstriction --> very very high bp

Front 30

moa of ace-i

Back 30

blocks ace, which converts aI to aII, also it prevents the breakdown of bradykinin

Front 31

moa of pde inhibitors

Back 31

decreased breakdown of camp --> increased ca entry into cells --> increased contractile fore
also --> vasodilation

Front 32

why are ace-i so useful in htn and in dm + htn

Back 32

there is no change in hr or co, no change in gfr b/c afferent and efferent arterioles are dilated equally
--> decreased intraglomerular pressure, very useful in diabetic nephropathy

Front 33

exmples of pde inhibitors used in cardiology

Back 33

milrinone
amrinone

Front 34

effects of ace-i in chf

Back 34

decreased pvr, decreased afterload and preload, increased co
increased co is counteracted by decreased pvr so bp doesn't go down (bp = co x pvr) unless pt is volume depleted

Front 35

uses for pde inhibitors

Back 35

chf if conventional vasodilation, dig, and diuretics don't work

Front 36

physiology behind why there is vasoconstriction in chf

Back 36

decreased co --> increased adrenergic stimulation and raas activation --> vasoconstriction

Front 37

downside of physiologic vasoconstriction in chf

Back 37

initially it is beneficial b/c there is increased preload b/c of venous constriction and bp is also maintained.
eventually, venous constriction --> too much vr --> increased pulmonary capillary pressure --> pulmonary edema
therefore, tx is vasodilation

Front 38

moa of ace-i

Back 38

blocks ace, which converts aI to aII, also it prevents the breakdown of bradykinin

Front 39

why are ace-i so useful in htn and in dm + htn

Back 39

there is no change in hr or co, no change in gfr b/c afferent and efferent arterioles are dilated equally
--> decreased intraglomerular pressure, very useful in diabetic nephropathy

Front 40

effects of ace-i in chf

Back 40

decreased pvr, decreased afterload and preload, increased co
increased co is counteracted by decreased pvr so bp doesn't go down (bp = co x pvr) unless pt is volume depleted

Front 41

side effects of ace-i

Back 41

cough
hypotension
hyperkalemia
--> renal failure in pts with bilateral renal artery stenosis

Front 42

what other medication is a good combo with ace-i

Back 42

thiazide diuretics

Front 43

aside from side effect profile (no cough) in what way is arb more effective than ace-i

Back 43

arb has a better reduction in bp b/c with ace-i, some aii can still form as ai is converted to aii by other enzymes

Front 44

moa hydralazine

Back 44

direct vasodilation at pre-capilllary arteriole level, no venous effects

Front 45

moa organic nitrates

Back 45

nitrates --> no --> activates cgmp --> sm muscle relaxation

Front 46

at low doses, effects of ng

Back 46

venous > arteriole dilation --> venous pooling, decreased vr, deccreased co; can also cause arterial dilation in coronary arteries

Front 47

at high doses, effects of ng

Back 47

widespread arteriole and venodilation --> systemic hypotension and reflex tachy

Front 48

where is the majority of na reabsorbed in the nephron

Back 48

65-70% reabsorbed in the pct

Front 49

how is na reabsorption accomplished in the tal

Back 49

n/k/cl transporter
tal is impermeable to h20 and hypotonic fluid forms

Front 50

what prompts na reabsorption in the dct
what else happens in the dct

Back 50

aldo
na is exchanged for k and h

Front 51

which part of the nephron is permeable to h20

Back 51

cct

Front 52

examples of loop diuretics

Back 52

furosemide
bumetamide

Front 53

moa loop diuretics

Back 53

acts on tal
inhibits the na/k/cl channel, so the fluid in the nephron is more hypertonic than it normally would be and the interstitium is hypotonic
by the time the fluid reaches the cct, the gradient for water reabsorption is diminished and diuresis occurs

Front 54

which diuretic class is still effective in renal insufficiency

Back 54

loop diuretics

Front 55

side effects of loop diuretics

Back 55

hypovolemia
hypokalemia
metabolic alkalosis
hypomag
ototoxicity

Front 56

explain why hypokalemia occurs in loop diuretic use

Back 56

because there is more na in the dct, the na-k/h exchanger is activated by a higher na concentration gradient... more k and h are lost through excretion
also, volume contraction occurs activating raas --> aldo activation --> h/k excretion by activating na-k/h transporter

Front 57

explain why metabolic alkalosis occurs in loop diuretic use

Back 57

increased h excretion at dct b/c of aldo
contraction alkalosis (increased nahco3 reabsorption by pct is promoted by decreased intravascular volume)

Front 58

moa thiazide diuretics

Back 58

blocks the na/cl cotransporter in the dct

Front 59

cardiac effects of thiazides

Back 59

initially, decreased co d/t hypovolemia without change in svr
later, co returns to nml b/c svr decreases through vasodilation (mech unkwn)

Front 60

what effect does renal failure have on thiazide use

Back 60

won't be effective if gfr <25

Front 61

which drug class are thiazides commonly combined with

Back 61

loop diuretics
they work at sequential regions in the nephron for synergistic effects

Front 62

side effects of thiazide use

Back 62

hypokalemia
metabolic alkalosis
hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia
hyponatremia

Front 63

why do hypokalemia and metabolic alk occur with thiazide use

Back 63

increased amt of na enters in the cct b/c of decreased reabsorption in the dct, so there is an increased activation of na-k/h exchanger --> increased k and h excretion
also, contraction alkalosis and activation of raas from volume contraction

Front 64

why does hyponatremia occur in thiazide use

Back 64

cont'd na excretion and free water consumption

Front 65

moa k sparing diuretics

Back 65

aldo agonists (spironolactone)
or direct inhibition of na-k/h exchanger in the dct (triampterene and amiloride)

Front 66

classes of antithrombotic drugs

Back 66

salicylates (asa), thienopyridines (clopidogrel/plavix), GP IIb/IIIa inhibitors (abciximab, eptifibatide)

Front 67

moa asa

Back 67

blocks formation of txa2 by acetylating cox-1

Front 68

uses of asa

Back 68

ua
mi
stable angina, icehmic strokes to prevent future strokes
s/p cabg

Front 69

what is the recommendation for using asa

Back 69

use in men and wmoen >50 yo with more than 1 cardiac risk factor
also use in pts with dm + 1 other risk factor

Front 70

use of asa in a-fib

Back 70

not as effective as warfarin

Front 71

adverse effects of asa

Back 71

dyspepsia
nausia
gib
ich
allergy
asthma exacerbations can exarcebate gout by competing with uric acid in pct of kidney during excretion

Front 72

example of thienopyridine

Back 72

clopidogrel (plavix)

Front 73

moa clopidogrel

Back 73

inhibits adp mediated plt activation

Front 74

time till onset of action of clopidogrel

Back 74

2-4 days

Front 75

uses of clopidogrel

Back 75

use in pts w asa allergy s/p stent
clopidogrel + asa s/p ua or stemi

Front 76

adverse effects of clopidogrel

Back 76

dyspepsia
diarrhea

Front 77

moa gp iib/iiia inhibitors

Back 77

inhibits plt aggregation

Front 78

uses of gp iib/iiia inhibitors

Back 78

improved outcomes in pci and high risk acs

Front 79

side effects of gp iib/iiia inhibitors

Back 79

bleeding
thromobcytopenia

Front 80

meds used for anticoagulation

Back 80

ufh
lmwh
warfarin
direct thrombin inibitors

Front 81

moa ufh

Back 81

associates with AT III, preventing the formation of thrombin from prothrombin, therefore preventing the conversion of fibrinogen to fibrin
also binds and blocks vwf

Front 82

uses of ufh

Back 82

ua
ami p thrombolytic tx
pe/dvt

Front 83

adverse effects of heparin

Back 83

osteoporosis
hit
bleeding

Front 84

what are the different types of hit

Back 84

1, thrombocytopenia from direct heparin induced plt aggregation; asx, dose-dependent; doesn't require cessation of tx
2, life-threatening bleeding and thrombosis occurring secondary to formation of ab vs heparin-plt complexes

Front 85

tx of life threatening hit

Back 85

immediate cessation of heparin products, substitute for a direct thrombin inhibitor to prevent more thrombosis

Front 86

moa lmwh

Back 86

interacts with AT III but preferentially inhibits factor Xa more potently than it blocks thrombin formation

Front 87

benefits of lmwh over ufh

Back 87

less rate of hit
better anti-coagulation effects
more predictable bioavailability
longer half-life for 1x day dosing

Front 88

how to check efficacy of lmwh

Back 88

factor Xa assay (usually only done in pts with renal failure)

Front 89

indications for lmwh

Back 89

dvt proph s/p hip, knee, abd surgery
tx of dvt/pe
acs management

Front 90

ex of direct thrombin inhibitors

Back 90

argatroban
luperidan

Front 91

moa direct thrombin inhibitors

Back 91

inhibits circulating and bound thrombin independently of AT III

Front 92

uses of direct thrombin inhibotors

Back 92

used to maintain anticoagulation and prevent thrombus formation in hit

Front 93

moa warfarin

Back 93

antagonizes enzyme involved in vitamin k metabolism

Front 94

which factors are affected by warfarin

Back 94

proteins c and s
coag factors 2, 7, 9, 10

Front 95

onset of warfarin

Back 95

takes 2-7 days to work