Cardiovascular drugs Flashcards

1
Q

MOA antiplatelet drugs

A

aspirin irreversibly acetylates COX preventing formation of thromboxane A2 thus inhibiting platelet aggregation

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2
Q

when is aspirin used

A

in low dose (75 mg/24h) for secondary prevention following MI, TIA/stroke and patients with angina, peripheral vascular disease. sometimes primary

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3
Q

which drugs cause less gastric irritation aspirin (antiplatelet) or clopidogrel etc (ADP receptor antagonists)

A

clopidogrel

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4
Q

examples of ADP receptor antagonists

A

(antiplatelets)- clopidogrel, prasugrel- block platelet aggregation. used if intolerant to aspirin

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5
Q

what role do glycoprotein IIB/IIIa antagonists have

A

unstable angina/ MI

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6
Q

example glycoprotein IIb/IIIa

A

tirofiban

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7
Q

which anticoag is used in AF and name another instance where used

A

warfarin; in those patients with mechanical valves

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8
Q

what are the newer oral agents

A

Xa inhibitors- apixaban; direct thrombin inhibitors- dabigatran. don’t need therapeutic monitoring

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9
Q

when is LMWH used

A

in ACS

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10
Q

what are alternative anticoags (not newer therapies)

A

parenteral fondaparinux (Xa inhibitor) or bivalirudin (thrombin inhibitor)

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11
Q

MOA b blockers

A

blocks adrenaline and NA on B adrenoceptors thus antagonising sympathetic nervous system

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12
Q

what does b1 receptor blockers cause in inotropic and chronotropic of heart

A

decreases inotropic and chronotropic - pulse decreases due to the decreased firing of SA node.

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13
Q

what does b2 receptor blockers induce

A

peripheral vasoconstriction and bronchioconstriction

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14
Q

what is the action of b1 receptor

A

incr chronotropic effect (rate), incr ionotropic effect (strength contractibility), increase renin secretion, increase ghrelin secretion(stomach)

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15
Q

what is the action of b2 receptor

A

smooth muscle relaxation, dilation of arteries to skeletal muscle, relaxation bronchioles, inhibit histamine secretion etc

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16
Q

what is an adrenergic receptor

A

GPCR receptors activated by adrenaline and noradrenaline

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17
Q

B blockers vary in their selectivity true or false

A

true

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18
Q

is propranolol selective

A

no

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19
Q

is bisoprolol selective

A

relatively B1 selective

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20
Q

uses of B blockers

A

angina, hypertension, antidysrhythmic, post MI, heart failure

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21
Q

contraindications of b blockers

A

asthma, COPD, heart block

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22
Q

caution use of B blockers, which can be used

A

heart failure. carvediol (and bisoprolol) can be used

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23
Q

side effects of B blockers

A

lethargy, erectile dysfunction, nightmares, headache

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24
Q

which type of diuretic is used in heart failure give example and MOA

A

loop diuretic- inhibits Na/2Cl/K co transporter eg furosemide

25
Q

what type of diuretic is used in hypertension give example and MOA

A

thiazide, inhibit Na/Cl cotransporter. bendroflumethiazide

26
Q

side effects of loop diuretics

A

dehydration, decr K, decr Ca, ototoxic

27
Q

side effects of thiazides

A

decr K, incr Ca, decr Mg, incr urate (+- gout), impotence

28
Q

example of K sparing diuretic

A

amiloride, spironolactone

29
Q

side effect amiloride

A

incr K, GI upset

30
Q

what are vasodilators used in

A

heart failure, IHD, hypertension

31
Q

examples of vasodilators

A

nitrates, prazosin, hydralazine

32
Q

MOA of nitrates

A

DECREASE PRE LOAD. dilates veins and large arteries so decreasing filling pressure

33
Q

MOA of hydralazine

A

DECREASE AFTER LOAD. primarily dilates resistance vessels (used with nitrates), and decr BP

34
Q

MOA prazosin

A

alpha blocker. dilates arteries and veins

35
Q

MOA calcium channel blockers

A

reduce entry Ca2+- voltage sensitive channels in smooth muscle. this leads to coronary and peripheral vasodilatation, reducing coronary oxygen consumption

36
Q

what receptors do the calcium channel blockers work on

A

L type Ca2+ channels

37
Q

examples of dihydropyridines (Ca2+) and what is their principle action

A

nifedipine, amlodipine. peripheral vasodilators also dilate coronary arteries.

38
Q

what do dihydropyridines cause and what are they used alongside, and what for

A

reflex tachycardia used alongside B blockers. angina and hypertension

39
Q

examples of non dihydropyridines (ca2+) and action, what used for

A

verapamil, diltiazem. slow conduction at AV and SA. hyptertension, angina, dysrhythmias

40
Q

what must you not give with B blockers

A

verapamil- risk severe bradycardia and LVF

41
Q

side effects Ca channel blockers

A

flushes, headache, oedema, LV function decr, gingival hypertrophy

42
Q

contraindications of Ca blockers

A

heart block

43
Q

MOA digoxin

A

blocks Na/K pump. slows pulse in fast AF. weak+ve inotrope

44
Q

who are at risk of incr toxicity with digoxin

A

elderly, use lower doses

45
Q

side effects digoxin

A

any arrhythmia, nausea, decr appetite, yellow vision, confusion, gynaecomastia

46
Q

in digoxin toxicity what needs to be checked

A

K+, treat arrhythmias, consider DigiFab by IVI

47
Q

contraindications of use of digoxin

A

HCM (hypertrophic obstructive cardiomyopathy), WPW

48
Q

what are dihydropyridines eg nifedipine used for

A

hypertension and angina

49
Q

what are phenylalkalines eg verapamil used for

A

arrhythmias and angina

50
Q

what are benzothiapenes eg diltiazem used for

A

hypertension, angina, arrhythmias

51
Q

what is the basic MOA of a diuretic

A

traps ions in urine so H2O moves from blood into urine in osmotic shift

52
Q

where does furosemide act

A

thick ascending loop of henle

53
Q

where does bendroflumethiazide act

A

distal convoluted tubule

54
Q

where does spironolactone act

A

collecting tubule

55
Q

what can lead to decreased therapeutic index for drugs such as digoxin and amiodarone

A

hypokalaemia

56
Q

how do K sparing diuretics work

A

usually Na is trapped in the loop or DCT which leads to a high conc of Na and so enhances K loss. in K sparing, the Na reabsorption is blocked in the collecting duct uncoupling the membrane which usually works in K secretion thus blocking the secretion of K into the urine

57
Q

what receptor is responsible for Ca2+ release from sarcoplasmic reticulum in cardiomyocytes

A

ryanodine receptor

58
Q

what enzyme is inhibited by statins

A

HMG-CoA reductase. de novo synthesis of cholesterol in the liver increasing LDL receptor expression by hepatocytes leading to decr circulating LDL cholesterol

59
Q

side effects statin

A

muscle aches, abdo discomfort, incr transaminases