Cardiac Drugs

Front 1

Mannitol
type
MOA

Back 1

Osmotic diuretic.
Increases tubular osmolarity which produces increased urine flow

Front 2

Mannitol
Clinical use

Back 2

Use: shock, drug overdose, decrease intercranial pressure

Front 3

Mannitol:
SE/Tox

Back 3

Pulmonary edema
dehydration
Contraindicated to CHF, anuria

Front 4

Acetazolamide
Type
MOA

Back 4

Carbonic anhydrase inhibitor
causes self limited diuresis and reduction in total body HCO3
Acts at PCT

Front 5

Acetazolamide:
Clinical use

Back 5

Glaucoma
urinary alkanization
metaboilic alkalosis
altitude sickness

Front 6

Acetazolamide: SE/Tox

Back 6

Hyperchloremic metabolic ACIDOSIS
Neuropathy
NH3 tox
sulfa allergy

Front 7

Furosemide:
Type
MOA

Back 7

Sulfonamide loop diuretic
Inhibits co-transport system ((Na, K, 2Cl) of Ascending
LOP

Abolishes hypertonicity of medulla which prevents concentration of urine

Increases Ca excretion

Front 8

Furosemide:
Clinical use

Back 8

Edematous state--CHF, cirrhosis, nephrotic syndrome, PE

hypertension

Hypercalcemia

Front 9

Furosemide:
SE/ Tox

Back 9

OH DANG!!
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Front 10

Ethcrynic acid
type
MOA

Back 10

Phenoxyacetic acid derivative--NOT a sulfonamide

Same as furosemide

Front 11

Ethcrynic acid:
clinical use

Back 11

Diuresis in pts with allergy to sulfa drugs

Front 12

Ethcrynic acid: SE/ Tox

Back 12

Similar to furosemide
can be used in hyperuricemia, acute gout
NEVER used to treat gout

Front 13

Hydrochlorothiazide:
Type
MOA

Back 13

Thiazide diuretic
Inhibits NaCl reabsorption in early DT which reduces diluting capacity of nephron.

Decreases Ca excretion

Front 14

Hydrochlorothiazide:
Clinical use

Back 14

Hypertension
CHF
idiopathic hypercalciuria
nephrogenic diabetes insipidus

Front 15

Hydrochlorothiazide:
SE/Tox

Back 15

hyperGLUC!!!
Hypokalemic metabolic alkalosis
hyponatremia
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalcemia
Sulfa allergy

Front 16

K sparing diuretics

Back 16

K STAys!!!
Spironolactone
triamterene
Amiloride
eplereone

Front 17

K sparing diuretics
MOA

Back 17

Spironolactone--competitive aldosterone receptor antagonist in CCT

Triamterene, amiloride--block Na channels in CCT

Front 18

K sparing diuretics:
Clinical use

Back 18

Hyperaldosteronism
K depletion
CHF

Front 19

K sparing diuretics:
Tox

Back 19

Hyperkalemia
endocrine effects (spironolactone causes gynecomastia)

Front 20

Effects of Diuretics:
Who causes what?

1) urine NaCl
2) Urine K
3) blood pH
4) Urine Ca

Back 20

1) increase-all diuretics (carbonic anhydrase inhibitors, loop diuretics, thiazides, K sparing)

2)increase--all except K sparing

3) decrease/acidosis--carbonic anhydrase inhibitors, K sparing
increase/alkalosis--loop diuretics, thiazides

4) increase-loop diuretics
decrease-thiazides

Front 21

Hydralazine:
type
MOA

Back 21

vasodilator

increases cAMP which increases smooth muscle relaxation. So, arterioles vasodilate > veins whihc reduces afterload

Front 22

Hydralazine
Clinical use

Back 22

Severe hypertension
CHF

Front 23

Hydralazine
SE/TOX

Back 23

Compensatory tachycardia
fluid retention
Lupus-like syndrome

Front 24

name Ca channel blockers

Back 24

Nifedipine
Verapamil
Diltiazem

Front 25

Nifedipine Verapamil Diltiazem:
type
MOA

Back 25

Ca channel blockers

Block voltage dependent L type ca channels of cardiac and smooth muscle which results in reduced muscle contractility

Vascular SM: N>D>V
Heart: V>D>N

Front 26

Nifedipine Verapamil Diltiazem:
Clinical Use

Back 26

Hypertension
angina
arrythmias (not N)

Front 27

Nifedipine Verapamil Diltiazem:
SE/Tox

Back 27

Cardiac depresion
peripheral edema
flushing
dizziness
constipation

Front 28

Name ACE inhibitors

Back 28

Captropil, Enalpril, Lisinopril

Front 29

Captropil, Enalpril, Lisinopril:

type
MOA

Back 29

ACE inhibitors

Inhibit ACE, reduce Ang II, prevent inactivation of bradykinin (potent vasodilator)

increased renin release dt loss of feedback

Front 30

Captropil, Enalpril, Lisinopril:
Clinical use

Back 30

Hypertension
CHF
diabetic renal disease

Front 31

Captropil, Enalpril, Lisinopril:
SE/Tox

Back 31

CAPTOPRIL
Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), rash, Increased renin, Lower Ang II levels AND hyperkalemia

Front 32

Nitroglycerin, isosorbide Dinitrate

MOA

Back 32

vasodilate: release NO to Smooht muscle which increases cGMP and smooht muscle relaxation

Effect: veins >> arteries

Front 33

Nitroglycerin, isosorbide Dinitrate:
Clinical use

Back 33

Angina
PE
aphrodisiac, erection enhancer

Front 34

Nitroglycerin, isosorbide Dinitrate

Back 34

tachycardia
hypotension
HA
Monday dz in industrial exposure--develop tolerance for vasodilating effect during week and loss of tolerance during weekend with resulting SE

Front 35

Antianginal therapy:
1) what is used?
2) Goal

Back 35

1) nitrates, B-blockers, and a combo of both

2) reduce myocardial O2 (MVO2) use by decreasing one of the determinants of MVO2--end diastolic volume, BP, heart rate, contractility, ejection time

Front 36

Anginal therapy: nitrates (affect preload)
EDV
BP
Contractility
HR
Ejection time
MVO2

Back 36

dec
dec

inc (reflex)
inc (reflex response)
dec
dec

Front 37

Anginal therapy: B-blockers (affect afterload)
EDV
BP
Contractility
HR
Ejection time
MVO2

Back 37

inc
dec
dec
dec
inc
dec

Front 38

Anginal therapy: nitrates + B-blockers
EDV
BP
Contractility
HR
Ejection time
MVO2

Back 38

no effect or dec
dec
little/none
dec
little/no
very dec

Front 39

Cardiac glycosides
name
Availability,%protein bound, half-life, excretion

Back 39

digoxin
bioavailability-75%
protein bound-20-40%
half life-40hours
urinary excretion

Front 40

Digoxin:
type
MOA

Back 40

glycoside
inhibits Na/K ATPase of cell membrane which causes an increase in cellular Na.

Na-Ca antiport does not fxn as well which causes an increase in intracellular Ca...all of this leads to positive ionotropy

May cause increased PR, decreased QT, scooping of ST, and T wave inversion

Front 41

Digoxin--
clinical use

Back 41

CHF-increase contractility
AFib-decrease conduction at AV node

Front 42

Digoxin--
SE/Tox

Back 42

N/V/D
Blurry yellow vision
Arrythmias

Front 43

Digoxin--
How are SE/Toxicity changed?

Back 43

Tox of digoxin are increased by:
renal failure,
hypokalemia (potentiates drugs effect)
quinidine--decreases drug clearance and displaces dig from tissue binding sites

Front 44

Digoxin--antidote

Back 44

Slowly normalize K
lidocaine
cardiac pacer
anti-dig Fab fragments

Front 45

Antiarrythmics
These are...?

Back 45

Na channel blockers (Class Ia, Ib, Ic)

B blockers (Class II)-propanolol, esmolol, metoprolol, atenolol, timolol

K channel blockers (Class III)Sotalol, ibutilide, bretylium, amiodarone, dofetilide

Ca channel blockers (Class IV) verapamil, diltiazem

Front 46

Beta Blockers

Back 46

B blockers (Class II)-propanolol, esmolol, metoprolol, atenolol, timolol

Front 47

K channel blockers

Back 47

K channel blockers (Class III)Sotalol, ibutilide, bretylium, amiodarone, dofetilide

Front 48

Na channel blockers Class Ia

Back 48

Queen Amy proclaims Discos Pyramide
Quinidine
Amiodarone
Procainamide
Disopyramide

Front 49

Na channel blockers Class Ib

Back 49

Lidocaine
mexiletine
tocainide

Front 50

Na channel blockers Class Ic

Back 50

Flecainide
encainide
Propafenone

Front 51

Na Channel Blocker Ia
Clinical effects of use?

Back 51

increase AP duration

increase effective refractory period

Increase QT

Affect both atrial and ventricular arrythmias

Front 52

Na channel blockers Ia:
Tox/SE

Back 52

quinidine-cinchonism (HA, tinnitus, thrombocytopenia, Torsades de pointes dt increased QT)

procainamide--reversible SLE like syndrome

Front 53

Na Channel Blockers : Class Ib
clinical effects and when to use

Back 53

decrease AP

affect ischemic or depolarized Purkinje and ventricular fiber

Useful in acute ventricular arrythmias (especially post MI) and in digitalis induced arrythmias

Front 54

Na channel blockers : Class Ib
SE/Tox

Back 54

Local anasthetic
CNS stimulation/depression
CV depresion

Front 55

Na channel blockers: Class Ic
clinical use or effect

Back 55

No effect on AP duration

Useful:
in VTachs that progress to VF
intractable SVT

last resort in refractoryt tacharrythmias

Front 56

Na channel blocker: Class Ic
SE/Tox

Back 56

proarrythmic esp post MI (contraindicated)

Front 57

Beta blockers
class?
MOA

Back 57

Class II antiarrythmics

decrease: cAMP, Ca currents
Suppress abnormal pacemakers by decreasing slope of Phase4

AV node very sensitive--increase PR

Esmolol--short acting

Front 58

Beta blockers
SE/Tox

Back 58

Impotence
exacerbation of asthma

CV effects--bradycardia, AV block, CHF

CNS effects-sedation, sleep alterations

May mask signs of hypoglycemia

Front 59

K channel blockers
class?
MOA/Clinical effects

Back 59

Antiarrythmics, Class III

Increase duration of AP, refractory period, QT

use when other antiarrythmics fail

Front 60

K channels blockers
Tox:
Sotalol

Back 60

torsades
excessive Beta block

Front 61

K channels blockers
Tox:ibutilide

Back 61

torsades

Front 62

K channels blockers
Tox:bretylium

Back 62

new arrythmias,
hypotension

Front 63

K channels blockers
Tox:amiodarone

Back 63

Pulmonary fibrosis
corneal deposits
skin deposits/photodermatitis
neurological effects
constipation
CV effects--bradycardia, heart block, CHF

REMEMBER:YOU MUST CHECK LFT, PFT, TFT
hepatotoxic
hypo/hyperthyroidism
pulmonary fibrosis

Front 64

Ca channel blockers
class
MOA/effect

Back 64

class IV

Primarily affect AV nodal cells

Dec conduction velocity,

Inc ERP, PR,

Prevent nodal arrythmias (SVT)

Front 65

ca channel blockers
Tox

Back 65

Constipation
flushing
edema
CV effects--CHF, AV block, sinus node depression

Front 66

Verapamil
Class, MOA, Tox

Back 66

Ca channel blocker

Front 67

diltiazem:Class, MOA, Tox

Back 67

ca channel blocker

Front 68

Sotalol:Class, MOA, Tox

Back 68

K channel blocker

Front 69

ibutilide:Class, MOA, Tox

Back 69

K channel blocker

Front 70

bretylium:Class, MOA, Tox

Back 70

K channel blocker

Front 71

amiodarone:Class, MOA, Tox

Back 71

k channel blocker
Na channel blocker, IA

Front 72

dofetilide:Class, MOA, Tox

Back 72

k channel blocker

Front 73

Quinidine Class, MOA, Tox

Back 73

Na channel, IA

Front 74

Procainamide Class, MOA, Tox

Back 74

Na channel, IA

Front 75

Disopyramide Class, MOA, Tox

Back 75

Na channel, IA

Front 76

Lidocaine Class, MOA, Tox

Back 76

Na channel, IB

Front 77

Mexiletine Class, MOA, Tox

Back 77

na channel, IB

Front 78

Tocainide Class, MOA, Tox

Back 78

Na channel, IB

Front 79

Flecainide Class, MOA, Tox

Back 79

Na channel, IC

Front 80

Encainide

Back 80

Na channel, IC

Front 81

Propafenone

Back 81

Na channel, IC

Front 82

Catopril?

Back 82

ACE I

Front 83

Enalapril?

Back 83

ACE I

Front 84

Lisinopril?

Back 84

ACE I

Front 85

Adenosine
family
use

Back 85

antiarrythmics

drug of choice in diagnosing/abolishing nodal arrythmias

Front 86

Adenosine:
effect of---
K

Back 86

(K)--Depresses ectopic pacemakers especially in digoxin tox

Front 87

Adenosine: effect on (Mg)

Back 87

(Mg)--Effective in torsades de pointes and dig tox

Front 88

Lipid Lowering agents

GO MEMORIZE THE TABLE ON P 319!!!!!!!!!!!

Back 88

HMG-CoA reductase inhibitors (statins)

Niacin

Bile acid resins (cholestyramine, colestipol)

Cholesterol absorption blocker (Ezetimibe)

Fibrates--names end in fibrate

Front 89

Statins??

Back 89

HMG-CoA reductase inhibitors

Front 90

Cholestyramine?

Back 90

Bile acid resin

Front 91

Colestipol??

Back 91

Bile acid resin

Front 92

Ezetimibe??

Back 92

cholesterol absorption blocker

Front 93

Gemfibrozil

Back 93

Fibrate

Front 94

hydrochlorothiazide:
family
SE

Back 94

diuretic

hypokalemia
slight hyperlipidemia
hyperuricemia
lassitude
hypercalcemia
hyperglycemia

Front 95

Loop diuretics: SE

Back 95

Potassium wasting
metabolic alkalosis
hypotension
ototoxicity

Front 96

Clonidine
Family
SE

Back 96

Sympathoplegics
Dry mouth
sedation
severe rebound HPT

Front 97

Methyldopa:
family
SE

Back 97

Sympathoplegics

Sedation
positive Coombs test

Front 98

Hexamethonium:
family
SE

Back 98

Sympathoplegics
Severe orthostatic hypotension
blurred vision
constipation
sexual dysfunction

Front 99

reserpine:
family
SE

Back 99

Sympathoplegics

Sedation
depression
nasal stuffiness
diahrrea

Front 100

Guanethidine:
family
SE

Back 100

Sympathoplegics

Hypotension: orthostatic, exercise
sexual dysfunction
diarrhea

Front 101

prazosin:
family
SE

Back 101

Sympathoplegics

1st dose orthostatic hypotension
dizzy
HA

Front 102

beta blockers
SE

Back 102

Impotence
Asthma
CV effects--bradycardia, CHF, AV block

CNS effects--sedation, sleep alterations

Front 103

Vasodilators

Back 103

Hydralazine
Minoxidil
Nifedipine
Verapamil (ca channel too)
Nitroprusside

Front 104

Hydralazine
family
SE
notes on usage

Back 104

vasodilators

nausea
HA
lupus like Syn
reflex tach
angina
salt retention

use with B blocker to prevent reflex tach

use with diuretic to block salt retention

Front 105

Minoxidil
family
SE
notes on use

Back 105

vasodilators

Hypertrichosis
pericardial effusion
reflex tach
angina
salt retention

use with B blocker to prevent reflex tach

use with diuretic to block salt retention

Front 106

nifedipine, verapamil
family
SE

Back 106

vasodilators

dizzy
flushing
constipation (verapamil)
nausea

Front 107

Nitroprusside
family
SE

Back 107

vasodilators

cyanide toxicity--releases CN

Front 108

ACE I

Back 108

captopril, enalpril, lisinopril

Front 109

Captropil
family
SE

Back 109

H-CAPTOPRIL

Front 110

Angiotensin II receptor inhibitors

Back 110

losartan

Front 111

Losartan
family
SE

Back 111

Angiotensin II receptor inhibitors

fetal renal tox

hyperkalemia