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Step 1 - Pharm > cardiac pharm > Flashcards

cardiac pharm Flashcards

1
Q

drugs for essential hypertension

A

diuretics, ACEi, ARBs, CCBs

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2
Q

drugs for hypertension in CHF

A

diuretics, ACEi, ARBs, CCBs B-blockers (conpensated CHF only), K sparing diuretics

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3
Q

drugs for hypertension in DM

A

diuretics, ACEi, ARBs, CCBs, alpha blockers

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4
Q

reason for giving ACEi to DM pts

A

protective against diabetic nephropathy

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5
Q

-dine drugs

A

CCBs

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6
Q

CCB Mechanism

A

block voltage gated L-type Ca channels in cardiac and smooth muscles and reduce muscle contactability

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7
Q

CCB NOT to be used in arrythmia

A

nifepidine

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8
Q

tox of CCBs

A

cardiac depression,AV block, peripherial edema, flushing dizzyness, constipation

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9
Q

hydralazine MOA

A

increase cGMP –> smooth muscle relaxation –> vasodilates arterioles –> reduces afterload

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10
Q

hydralazine use

A

severe hypertension, CHF.. Coadministered with B blocker to prevent reflex tachycardia

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11
Q

first line therapy for hypertension in pregnancy

A

hydralazine (with methyldopa)

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12
Q

treatment for malignant hypertension

A

nitroprusside, CCBs, labetalol, fenoldapam

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13
Q

tx of hydralazine

A

compensitory tachycardia, fluid retention, nausea, headache, angina, Lupus-like syndrome

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14
Q

Tox of nitroprusside

A

cyanide poisoning

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15
Q

MOA of nitroprusside

A

increase GMP by direct release of NO.

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16
Q

moa of fenoldapam

A

D1 receptor agonist, conorany, peripheral, renal and splachnic vasodilation

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17
Q

“monday disease”

A

development of tolerance during the week for isosorbide. loss of tolerance during the weekend. Start back up with tachycardia, dizzyness and headache

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18
Q

drugs NOT to be used in angina

A

pindolol and acebutolol

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19
Q

antilipid with the best effect on LDL

A

statins

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20
Q

MOA of statin

A

inhibit conversion of HMG-CoA to mevalonate

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21
Q

Side effects of statins

A

hepatotox, rhabdo

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22
Q

antilipid with the best effect on HDL

A

niacin

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23
Q

MOA of niacin

A

inhibits lipolysis, reduces VLDL circulation

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24
Q

Side effects of niacin

A

flushing, hyperglycemia, hyperuricemia

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25
Q

Bile acid resins examples

A

cholestyramine, colestipol, colsevelam

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26
Q

Bile acid resin effect

A

moderate lowering of LDL, slightly higher HDL and TGs

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27
Q

Bile acid MOA

A

prevent intestinal reaborption of bile acids - liver must use cholesterol to make more

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28
Q

Bile acid side effects

A

taste bad and screws with your gut. malaboprtion of fat soluable vitamins. cholesteral gallstones

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29
Q

ezetimibe effect

A

moderate lower LDL

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30
Q

ezetimibe MOA

A

prevent cholesteral reabsorption at SI brush border

31
Q

ezetimibe side effects

A

rare increase in LFTs, diarrhea

32
Q

fibrate effects

A

large reduction in TGs

33
Q

fibrate MOA

A

upregulate LPL, clearing TGs

34
Q

firate side effects

A

myositis, hepatotox, cholesterol gallstones

35
Q

MOA of digoxin

A

direct inhibition of Na/K ATPase leading to direct inhibition of Na/Ca exchangers. increase in intracelluar Ca –> increase contractability.

Also stimulates Vagus nerve to slow HR

36
Q

use of digoxin

A

CHF, Afib (slow conduction at AV and depression of SA)

37
Q

tox of digoxin

A

cholinergic (N/V, diarrha, blurry yellow vision)

increasedPR, lower QT, T wave inversion,a rrythmia - AV block

38
Q

poor prognostic indicator in digoxin tox

A

hypokalemia

39
Q

antidote for dig tox

A

normallize K+, lidocaine, anti-digoxin fab fragments, Mg2+

40
Q

effect of Na+ channel blocker antiarrythmics (Class I)

A

slow or block conduction in abnormal pacemaker cels

41
Q

causes increased tox in class 1 antiarrythmics

A

low K

42
Q

class 1A antiarrythmics

A

Quinidine, Procainamide, disopyramide

43
Q

class 1A antiarrythmics action

A

increase AP duration, increase refreactory period, increase QT

44
Q

class 1A antiarrythmics use

A

A and V arrythmias. Ectopic supraventricular tachy and v tach

45
Q

quinadine tox

A

cinchoism

46
Q

procanamide tox

A

SLE-type syndrome

47
Q

disopyramide

A

Heart failure, thrombocytopenia, torsades de pointes

48
Q

class IB antiarrythmics effect

A

lower AP duration. affects aischemuc or depolarized purkinjie and ventriculartissue

49
Q

class IB antiarrythmics use

A

acute ventricular arrythmias (especially post-MI) and digitalis induced arrythmias

50
Q

class IB antiarrythmics

A

lidocaine, mexiletine, tocainide (phenytoin can be listed)

51
Q

tox of class IB antiarrythmics

A

CNS stimulation/depression, CV depression

52
Q

class IC antiarrythmics

A

flecainide, propafenone

53
Q

class IC antiarrythmics effect

A

useful in ventricular tachycardias that progress to VF and in tractable SVT - used as last resort in refractory tachy

54
Q

people NOT to use class IC antiarrythmics with

A

post-MI, structural heart disease

55
Q

class IC antiarrythmics tox

A

proarrythmic, significantly prologs refreactory period in AV node

56
Q

antiarrythmic beta blockers

A

metoprolol, proanolol, emolol, atenolol, timolol

57
Q

antiarrythmic beta blockers MOA

A

decreases SA and AV nodal activity by deceraseing cAMP and lowering Ca currents

58
Q

short acting antiarrythmic beta blocker

A

esmolol

59
Q

use of antiarrythmic beta blockers

A

Vtach, SVT, slowing ventricular rate during afib and a flutter

60
Q

tox of antiarrythmic beta blockers

A

impotence, worse asthma, bradycardia, CHF, sedation, may mask hypoglycemia

61
Q

side effect of metoprolol

A

dyslipidemia (treat OD with glucogon)

62
Q

can exacerbate vasospasm in prinzmetal’s

A

propanolol

63
Q

K+ channel blockers (Class III antiarythmics)

A

amidorone, ibutilide, dofeilite, soralol

64
Q

effect of Class III antiarythmics

A

increase AP duration, used when other antiarrythmics fail, increase QT interval

65
Q

tox of sotalol

A

torsades des pointes, excessive Beta blockade

66
Q

tox of amidorine

A

pulmonary fibrosis, hepatotox, hypothyroidism (check PFTs, LFTs, TFTs) corneal and skin deposits, neuro effects,bradycardia, AV block

67
Q

MOA of verapamil, diltiazem

A

CCB, lower conduction velocity, increase ERP and PR inverval, prevents nodal arrythmia

68
Q

tox of verapamil, diltiazem

A

constipation, flushing, edema, sinus node depression

69
Q

adenosine MOA

A

sends K out of cells - hyperpolarizes and lowering intracellular calcium,

70
Q

adenosine is the DOC for

A

supraventricular tachy (VERY short acting)

71
Q

T 1/2 for dig

A

40 hours

72
Q

blocks effects of adenosine

A

theophylline and caffiene

73
Q

Mg++ used for

A

torades des points and dig tox

Step 1 - Pharm (17 decks)

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