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Antianginal > Antianginal > Flashcards

Antianginal Flashcards

1
Q

Principles of treatment of CCS

A

Use of antiischemic or antianginal agents and prevention of adverse cardiovascular event

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2
Q

No donors

A

Glyceril trinitrate,isosorbide mononitrate

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3
Q

1st gen beta Andre preceptor antagonist

A

Propranalol

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4
Q

Non dihydropiridine calcium channel blockers

A

Verapamil, diltiazem

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5
Q

Late Na flow inhibitor

A

Ranolazine

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6
Q

Sinoatrial node inhibitor

A

Ivabradine

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7
Q

Hypolipidemic agents are

A

Atorvastatin,fenofibrate,ezetimibs,evolozumab

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8
Q

Drugs used for prevention of adverse cardiovascular event

A

Hypolipidemic agents,RAAS, antiplatelet,ACE inhibitor,ARB

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9
Q

Cause of angina

A

Disrupted balance of oxygen supply and consumption

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10
Q

To reduce angina

A

Reduce oxygen consumption or increase oxygen supply

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11
Q

Oxygen demand increases when

A

Increase in HR, Contractions,wall tension, Preload ,afterload

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12
Q

Decrease oxygen supply due to

A

Decreased vessel caliber,perfusion pressure and increased HR, ventricular wall tension

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13
Q

Oxygen consumption can be reduced through

A

Reduced preload, afterload and CMV

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14
Q

Increased oxygen supply can be done through

A

Coronary blood vessel dilation, negative chronotropy

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15
Q

Negative chronotropy gives

A

Prolonged diastolic filling,so more oxygen supply

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16
Q

Nitrates and dihydropiridine calcium channel blockers cause

A

Reflex tachycardia

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17
Q

NO donors cause

A

Venodilation, arterial dilation and coronary arterial dilation,so hypotensive and antianginal effect

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18
Q

Glyceril trinitrate,fast and short acting

A

1-3min start, duration 20-30min, sublingual,first pass effect, antianginal

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19
Q

Side effects of glyceril nitrate

A

Headache, hypotension,reflex tachycardia

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20
Q

ISMN,Long acting,6-8 hr

A

Prevention of angina attack, interactions with pde5inhibitors cause life threatening hypotensive reaction

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21
Q

Dihydropiridine drugs are

A

Vasoselective calcium channel blockers -vasodilation

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22
Q

Dihydropiridine drugs acts on peripheral arteries and

A

Coronary arteries,cause dilation and antianginal and hypotensive effect

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23
Q

Side effects of dihydropiridine calcium channel blockers

A

Headache,facial flushing, fatigue, peripheral edema, constipation

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24
Q

Vasospastic anginais same as

A

Princmetals angina

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25
Q

Clinical use of dihydropiridine drugs

A

Prevention or prophylaxis of angina attack and prevention of vasospastic angina attack

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26
Q

Non dihydropiridine calcium channel blockers are

A

Cardiodepressent and are non selective

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27
Q

Clinical use of both calcium rare same

A

Prevention of angina attack and vasospastic angina attack

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28
Q

Action of non dihydropiridine blockers

A

Reduce CMV, peripheral arterial dilation,coronary artery dilation,diastole prolongation and reduce AV conduction

29
Q

CCB acts on

A

L type voltage dependent calcium ion channels

30
Q

Undamaged endothelium releasing NO and PGI2

A

Inhibits platelets activation

31
Q

CCB s are

A

Metabolic poison , because it increases dependence on carbohydrate metabolism than FFA

32
Q

CcBs cause

A

Coronary and peripheral vasodilation, decrease heart contractility,,slowed AV nodal conduction and depressed SA node activity

33
Q

Beta blockers and verapamil interactions cause

A

Bradyarrythmia and if used parentaral asystole

34
Q

Inhibitors of cyp450

A

Macrolide antibiotics and grapefruit juice

35
Q

CCB intoxication cause

A

Hypotension and bradycardia and prolonged PR i,nausea, vomiting, metabolic acidosis and hyperglycaemia

36
Q

Dihydropiridine cause

A

Vasodilatory shock

37
Q

Verapamil and diltiazem cause

A

Vasodilatory and cardiogenic shock+bradycardia

38
Q

Bradycardia can be caused by

A

Sinus bradycardia, second or 3rd degree AV block or sinus arrest

39
Q

CCB doesn’t affect

A

QRS duration

40
Q

CCB toxicity can be treated by

A

Calcium chloride or calcium gluconate for cardiac contraction, insulin against hyperglycaemia, Epinephrine, dobutamine or isoproterenol against cardiogenic shock and phenylephrine and norepinephrine against vasodilatory shock

41
Q

HIET

A

High dose insulin euglycemic therapy

42
Q

BAB are

A

Cardiodepressent

43
Q

BAB action

A

Reduce CMV, prolonged diastole, reduce AV conduction

44
Q

Use of BAB

A

Prevention of angina attack

45
Q

Side effects of BAB

A

Bradycardia,AV block, bronchospasm, cold extremities

46
Q

NO modulators have reflex increase in

A

HR and contractility

47
Q

End diastolic volume and ejection fractions increase for

A

BAB and CCB

48
Q

Ivabradin

A

Inhibits na ion flow in 4th phase of AP in SA node

49
Q

Action of ivabradin

A

Dose dependent decrease of HR, prolonged diastole

50
Q

Use of ivabradin

A

In prevention or prophylaxis of stable angina attack

51
Q

Side effects of ivabradin (SA node inhibitor

A

Photopsy(light phenomenon in the retina, bradycardia

52
Q

Ranolazine

A

Cause late blockade of na channels

53
Q

Ranolazine action

A

Indirectly reduces intracellular calcium ion concentration and therefore reduce myocardial diastolic tension,so decrease oxygen consumption,improves perfusion

54
Q

Atorvastatin action

A

g co A reductase inhibition +pleiotropic effects (plaque stabilization,,blocks synthesis of mevalonic acid in the liver, increase LDL receptor in liver and decrease LDL in plasma

55
Q

Atorvastatin

A

hMG co A reductase inhibition +pleiotropic effects (plaque stabilization,,blocks synthesis of mevalonic acid in the liver, increase LDL receptor in liver and decrease LDL in plasma

56
Q

Atorvastatin uses

A

Dyslipidemia, prevention of cardiovascular events

57
Q

Side effects of atorvastatin

A

Hepatic function impairment (hepatopathy )and myopathy

58
Q

Fibric acid derivatives

A

Fenofibrate

59
Q

PPAR alpha agonist

A

Fenofibrate

60
Q

Action of Fenofibrate

A

Activation of PPAR alpha leads to LPL gene expression ,lead serum LPL activation,lead to lipolysis, decrease TG and increase LDL receptor in liver

61
Q

Cholesterol absorption inhibitor

62
Q

Ezetimibe Acton

A

Blocks transport protein NPC1L1 in enterocyte villi-decrease cholesterol absorption (doesn’t affect fat sol but,TG or bile acids)-decrease LDL

63
Q

PCSK9 inhibitor

A

Evolozumab

64
Q

Evolozumab action

A

Inhibition of LDL receptor degrading enzymes

65
Q

Evolozumab action

A

Human IgG2 binds with PCS K9 affecting PCSK9 mediated degrading of LDL receptor in liver -decrease LDL naturally

66
Q

PCSK9

A

Proprotein convertase subtilisin/kexin type 9

67
Q

Vasospastic angina can be treated by

A

CCB and long acting organic nitrates

68
Q

Treatment of structural microvascular angia

A

BAB,ACE,statins

69
Q

Microvascular functional changes(vasospastic form treatment

A

Calcium CB,Long lasting organic nitrate

Antianginal (1 decks)

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