Z Cardiovascular Pharmacology

Front 1

essential hypertension rx

Back 1

diuretics
ACE inhibitors/ARBs

calcium-channel blockers

Front 2

antihypertensive therapy rx

CHF

Back 2

diuretics
ACE inhibitors/ARBs

beta blockers (compensated CHF)

K+ sparing diuretics

Front 3

antihypertensive therapy rx

diabetes

Back 3

ACE inhibitors/ARBs

calcium channel blockers

diuretics

beta-blockers

alpha-blockers

Front 4

_ are protective against diabetic nephropathy

Back 4

ACE inhibitors

Front 5

hydralazine moa (3)

Back 5

^ cGMP

--> smooth muscle relaxation

arterioles > veins

Front 6

hydralazine rx

Back 6

severe hypretension
CHF

hypertension in pregnancy

Front 7

hypertension in pregnancy rx

Back 7

hydralazine with methyldopa

Front 8

how is hydralazine administered?

Back 8

coadministered with a beta-blocker

to prevent reflex tachycardia

Front 9

hydralazine s/e

Back 9

compensatory tachycardia
(therefore: contraindicated
in angina/CAD)

fluid retention

nausea
headache

angina

lupus-like syndrome

Front 10

calcium channel blockers moa

Back 10

block voltage-dependent L-type calcium channels of

cardiac and smooth muscle

thereby reduce contractility

Front 11

calcium channel blockers clinical use

Back 11

angina

hypertension
arrhythmias (not nifedipine)
Raynaud's
Prinzmetal's angina

"a harp" with smooth muscle holding the strings taut. CCBs relax those strings.

Front 12

calcium channel blockers s/e

Back 12

AV block
cardiac depression

constipation
dizziness
peripheral Edema
flushing

AB, CD, C, D, E, F

Front 13

nitroglycerin
isosorbide dinitrate

moa

Back 13

release NO in smooth muscle
-->

^ cGMP -->

vasodilation

veins >> arteries

Front 14

nitroglycerin
isosorbide dinitrate

clinical use

Back 14

angina
pulmonary edema

Front 15

nitroglycerin
isosorbide dinitrate

s/e

Back 15

reflex tachycardia
hypotension
flushing
headache

"Monday disease"
--tachycardia
--dizziness
--headache

on industrial re-exposure after weekend

Front 16

malignant hypertension treatment

Back 16

nitroprusside
fenoldopam
diazoxide

Front 17

nitroprusside moa

Back 17

short-acting

direct release of NO -->
^ cGMP

Front 18

nitroprusside s/e

Back 18

cyanide toxicity

Front 19

fenoldopam moa

Back 19

D1 agonist

relaxes renal vascular smooth muscle

Front 20

diazoxide moa

Back 20

K+ channel opener

hyperpolarizes and relaxes vascular smooth muscle

Front 21

diazoxide s/e

Back 21

hyperglycemia

(reduces insulin release)

Front 22

myocardial O2 consumption is determined by (5)

Back 22

end diastolic volume
blood pressure
heart rate
contractility
ejection time

Front 23

antianginal therapy

Back 23

nitrates
beta blockers

or both!

-------------------
calcium channel blockers

Front 24

calcium channel blockers. compare with other anti angina drugs

Back 24

nifedipine is similar to nitrates in its effects

verapamil is similar to beta-blockers in its effects

Front 25

_ beta blockers are contraindicated in angina

Back 25

pindolol
acebutolol

partial beta-agonists

Front 26

nitrates' and beta-blockers' effects on the determinants of myocardial O2 consumption

Back 26

nitrates v preload;
beta-blockers v afterload

EDV v ^
BP v v

contractility ^ (reflex) v
HR ^ (reflex) v

ejection time v ^

Front 27

statins' effects: LDL, HDL, tri

Back 27

v v v ^ v

Front 28

niacin effects: LDL, HDL, tri

Back 28

v v ^ ^ v

Front 29

bile acid resins are

Back 29

cholestyramine
colestipol
colesevelam

Front 30

cholestyramine is a

Back 30

bile acid resin

Front 31

colestipol is a

Back 31

bile acid resin

Front 32

colesevelam is a

Back 32

bile acid resin

Front 33

ezetimibe is a

Back 33

cholesterol absorption blocker

Front 34

bile acid resins' effects:

LDL, HDL, tri

Back 34

v v slight ^ slight ^

Front 35

ezetimibe effects:

LDL, HDL, tri

Back 35

v v -- --

Front 36

fibrates' effects:

LDL, HDL, tri

Back 36

v ^ v v v

Front 37

which lipid drug increases HDL the most?

Back 37

niacin

Front 38

which lipid drug lowers LDL the most?

Back 38

statins

Front 39

which lipid drug lowers triglycerides the most?

Back 39

fibrates

Front 40

which lipid drug has no effect on HDL or triglycerides?

Back 40

ezetimibe

Front 41

niacin moa

Back 41

inhibits lipolysis in adipose

reduces hepatic VLDL secretion

Front 42

statins s/e

Back 42

hepatotoxicity (^ LFTs)

rhabdomyolysis

Front 43

niacin s/e

Back 43

flushed face
-- v by aspirin or long-term use

hyperglycemia
-- (acanthosis nigricans)

hyperuricemia
-- (exacerbates gout)

Front 44

this lipid lowering drug causes hyperuricemia

Back 44

niacin

Front 45

bile acid resins include

Back 45

cholestyramine
colestipol
colesevelam

Front 46

cholestyramine
colestipol
colesevelam

s/e

Back 46

bad taste

GI discomfort

v absorption of fat-soluble vitamins

cholesterol gallstones

Front 47

bile acid resins moa

Back 47

- intestinal reabsorption of bile acids

--> liver must use cholesterol to make more

Front 48

ezetimibe moa

Back 48

prevents cholesterol reabsorption

at small intestine brush border

Front 49

ezetimibe s/e

Back 49

rare ^ LFTs

Front 50

fibrates moa

Back 50

upregulate LPL -->

^ TG clearance

Front 51

fibrates' side effects

Back 51

myositis

hepatotoxicity (^ LFTs)

cholesterol gallstones

Front 52

lipid-lowering drugs that can cause cholesterol gallstones

Back 52

bile acid resins:
--cholestyramine
--cholestipol
--colesevelam

fibrates
--gemfibrozil
--clofibrate
--bezafibrate
--fenofibrate

Front 53

ryanodine moa

Back 53

a poison

inhibits calcium release from SR

Front 54

the cellular components involved in excitation-contraction coupling

Back 54

plasma membrane:

--Na+ / K+ ATPase

--Na+ - Ca++ exchanger

--voltage-gated (L-type) calcium channel


sarcoplasmic reticulum:

--calcium pump

--ryanodine receptors = calcium release channels

--calcium interaction with troponin-tropomyosin

Front 55

the major cellular mediator of calcium-induced calcium release

Back 55

ryanodine receptors (calcium release channels in the SR)

Front 56

beta1 receptors effects on the myocyte calcium system

Back 56

they're Gs

+ protein kinase A

phosphorylates
-- L-type Ca++ channels in the plasma membrane
--phospholamban

--> ^ intracellular Ca++ during contraction

Front 57

phospholamban function

Back 57

regulates the SR calcium pump

if dephosphorylated, it -'s the pump

Front 58

half-life of digoxin

Back 58

40 hours

Front 59

digoxin mechanism

Back 59

- Na+ / K+ ATPase

stimulates vagus nerve

Front 60

clinical use of digoxin

Back 60

CHF
-- ^ contractility

atrial fibrillation
-- depresses SA node
-- v conduction at AV node

Front 61

digoxin s/e

Back 61

cholinergic:
--n/v/d
--blurry yellow vision

^ PR
v QT
scooping
T-wave inversion
arrhythmia

hyperkalemia

Front 62

digoxin s/e's are worsened by...

Back 62

renal failure

hypokalemia

quinidine

Front 63

digoxin's s/e's are worsened by...

Back 63

renal failure (v excretion)

hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase)

quinidine
-- v digoxin clearance
-- displaces digoxin from tissue-binding sites

Front 64

antidote to digoxin toxicity

Back 64

slowly normalize K+
lidocaine
pacer
anti-dig Fab fragments
Mg++

stop taking it!

Front 65

class I antiarrhythmics mechanism (4)

Back 65

v conduction, especially in depolarized cells

v slope of phase 0 depolarization

^ threshold in abnormal pacemakers

selectively depress tissue that is frequently depolarized e.g. fast tachycardia

Front 66

class IA antiarrhythmics are...

Back 66

quinidine
procainamide
disopyramide

Front 67

class IA antiarrhythmics' effects on the action potential etc.

Back 67

^ AP duration

^ ERP

^ QT interval

Front 68

class IA antiarrhythmics rx

Back 68

atrial and ventricular arrhythmias

especially:

reentrant and ectopic SVT and VT

Front 69

class IA antiarrhythmics s/e

Back 69

thrombocytopenia
torsades de pointes

quinidine
--headache, tinnitus

procainamide
--reversible SLE-like syndrome

Front 70

class IB antiarrhythmics include...

Back 70

lidocaine
mexiletine
tocainide

phenytoin can also be a IB antiarrhythmic

Front 71

class IB antiarrhythmics rx

Back 71

ischemic or depolarized Purkinje and ventricular tissue

acute ventricular arrhythmias (especially post-MI)

digitalis-induced arrhythmias

Front 72

class IB antiarrhythmics s/e

Back 72

CNS stimulation/depression

cardiovascular depression

Front 73

all the class I antiarrhythmics are...

Back 73

local anesthetics

Front 74

class IC antiarrhythmics include...

Back 74

flecainide
encainide
propafenone

Front 75

class I antiarrhythmics:

for post-MI

contraindicated post-MI

Back 75

IB

IC

Front 76

class I antiarrhythmics effect on AP duration

Back 76

IA ^
IB v
IC --

Front 77

class IC antiarrhythmics rx (2)

Back 77

V-tachs that progress to V-fib

intractable SVT

used only as a last resort in refractory tachyarrhythmias

for patients without structural abnormalities

Front 78

class IC antiarrhythmics s/e

Back 78

proarrhythmic, esp. post-MI

significantly prolongs refractory period in AV node

Front 79

_ increases toxicity for all class I drugs

Back 79

hyperkalemia

Front 80

beta blockers mechanism as antiarrhythmics

Back 80

suppress abnormal pacemakers by

v slope of phase 4

AV node particularly sensitive, so ^ PR interval

Front 81

very short acting beta blocker

Back 81

esmolol

Front 82

clinical use of beta blockers

Back 82

V-tach
SVT

slowing ventricular rate during
atrial fibrillation and atrial flutter

Front 83

this beta blocker can cause dyslipidemia

Back 83

metoprolol

Front 84

metoprolol s/e

Back 84

dyslipidemia

Front 85

class III antiarrhythmics include

Back 85

sotalol
ibutilide
bretylium
dofetilide
amiodarone

Front 86

class III antiarrhythmics moa

Back 86

^ AP duration
^ ERP
^ QT interval

used when other antiarrhythmics fail

Front 87

these antiarrhythmics are listed as

^ AP duration
^ ERP
^ QT interval

Back 87

class IA

class III

Front 88

sotalol s/e

Back 88

torsades de pointes
excessive beta block

Front 89

ibutilide s/e

Back 89

ibutilide

Front 90

bretylium s/e

Back 90

new arrhythmias
hypotension

Front 91

amiodarone s/e

Back 91

pulmonary fibrosis

hepatotoxicity

hypothyroidism/hyperthyroidism

corneal deposits
skin deposits (blue/gray)
consipation

bradycardia
heart block
CHF

Front 92

amiodarone has class _ effects because _

Back 92

I, II, III, III

alters the lipid membrane

Front 93

alprostadil is a _. can be used to _

Back 93

PGE1

keep ductus arteriosus open

Front 94

class IV antiarrhythmics

Back 94

verapamil
diltiazem

Front 95

class IV antiarrhythmics moa

Back 95

v conduction velocity
^ ERP
^ PR interval

Front 96

class IV antiarrhythmics are used for _

Back 96

prevention of nodal arrhythmias e.g. SVT

Front 97

class IV antiarrhythmics s/e

Back 97

constipation
flushing
edema

CHF
AV block
sinus node depression

Front 98

adenosine moa

Back 98

^ K+ out of cells --> hyperkpolarization

v Ca++ coming in

Front 99

adenosine use

Back 99

drug of choice for

supraventricular tachycardia

Front 100

adenosine s/e

Back 100

"c h f"

chest pain
hypotension
flushing

Front 101

effects of adenosine are blocked by _

Back 101

theophylline, which is a competitive inhibitor

Front 102

K+ use as an antiarrhythmic

Back 102

depresses ectopic pacemakers in hypokalemia e.g. digoxin toxicity

Front 103

Mg++ is effective as an antiarrhythmic for ...

Back 103

torsades de pointes

digoxin toxicity