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Pharma 2 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Vasospastic angina is caused by

A

Functional changes in epicardial arteries

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2
Q

Stable angina is

A

Obstructive coronary artery disease

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3
Q

CCS is due to

A

Structural or functional changes in epicardial or cardiac arteries

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4
Q

Treatment method for CCS is

A

Use of antiischemic agents and prevention of adverse cardiovascular events

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5
Q

Antiischemic is same as

A

Antianginal

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6
Q

NO donors are

A

Glyceril trinitrate and isosorbide mononitrate

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7
Q

1st gen BAB

A

Propranalol

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8
Q

Non dihydropiridine calcium channel blockers

A

Verapamil and diltiazem

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9
Q

SA node inhibitor

A

Ivabradine

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10
Q

Late sodium flow inhibitors

A

Ranolazine

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11
Q

Hypolipidemic agents are

A

Atorvastatin, fenofibrate,ezetimibs, evolozumab

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12
Q

Cause of angina

A

Disrupted balance between oxygen supply and oxygen consumption in myocardium

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13
Q

To restore balance

A

Reduce oxygen consumption or increase oxygen supply

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14
Q

Decrease in blood supply can be caused by

A

Increase HR, increase ventricular wall tension, decrease in vessel caliber, decrease in perfusion pressure

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15
Q

Increased oxygen demand can be caused by

A

Increase in HR, ventricular wall tension,heart contractility, increase in preload and afterload

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16
Q

Antiischemic activity is ensured by

A

Reduction of preload , afterload and CMV (all these reduce oxygen demand)

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17
Q

Increase Oxygen supply can be provided by

A

Coronary blood vessel dilation and negative chronotropy (HR)-increase in diastolic filling time)

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18
Q

Nitrates and CCB (dihydropiridine) can also cause

A

Reflex tachycardia like doxazosin

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19
Q

NO provides peripheral arterial dilation in

A

High doses,in low doses only venodilation

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20
Q

NO dilates veins , peripheral arteries and coronary artery so it has

A

Antianginal and hypotensive effect

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21
Q

NO increases

A

cGMP-causes dephosphorylation of myosin light chain-dilation

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22
Q

Fast and short acting organic nitrate

A

Glyceril trinitrate (action onset in 1-3 minutes, duration of action 20 to 30 min)

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23
Q

Use of glyceril trinitrate

A

Angina attack

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24
Q

Long acting isosorbide mononitrate (6-8hr duration of action) use

A

Prevention of angina attack

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25
Q

Nitrates free interval needed

A

10 to 12 hr

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26
Q

SE of glyceril trinitrate

A

Headache , hypotension, reflex tachycardia

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27
Q

Dihydropiridine blockers action

A

Dilates peripheral arteries and coronary arteries -antianginal and hypotensive effect

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28
Q

Use of dihydropiridine blockers

A

Prevention of angina attack, prevention of vasospastic angina attack, arterial hypertension

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29
Q

SE of dihydropiridine blockers

A

Headache, facial flushing, fatigue, peripheral edema ankles, constipation

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30
Q

Non dihydropiridine blockers are

A

Non vasoselective and has cardiodepressent effect

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31
Q

Non dihydropiridine blockers

A

Reduce CMV,dilates peripheral and coronary artery,prolongs diastole,reduce AV conduction (antiarrhythmic)

32
Q

Use of Non dihydropiridine calcium channel blockers

A

Prevention of angina attack and vasospastic angina attack

33
Q

CCB suppress

A

L type voltage dependent calcium channel

34
Q

L type channel have

A

Slow or prolonged action but activates quickly, slowly inactive

35
Q

NO and PGI2 inhibits

A

Platelet activation

36
Q

CCB are metabolic poisons because

A

It increases heart dependence on carbohydrate metabolism than usual fat metabolism+inhibition of insulin release -difficult to use carbohydrates during shock

37
Q

Life threatening bradyarrythmia is caused in interaction between

A

Beta blockers and verapamil,on parentaral administration can also cause asystole

38
Q

Macrolide antibiotics and grapefruit juice can increase the amount of

A

Calcium antagonist by inhibing CYP 450 enzyme CYP 3A4

39
Q

Dihydropiridine+ACE inhibitors and/or ARB combined overdose cause

A

Hypotension

40
Q

Calcium antagonist intoxication cause

A

Bradycardia and hypotension

41
Q

Dihydropiridine cause —-shock

A

Vasodilatory shock

42
Q

Verapamil and diltiazem cause —- shock

A

Combined vasodilatory and cardiogenic shock

43
Q

Verapamil and diltiazem can also cause

A

Sinus bradycardia,2nd and 3rd degree AV block, sinus arrest

44
Q

Verapamil affect

A

PR interval even in Therapeutic dose

45
Q

Verapamil

A

Prolongs PR interval

46
Q

CCB intoxication non cardiacanifedtations are

A

Hyperglycaemia, nausea, vomiting, metabolic disorders

47
Q

Hyperglycaemia is due to

A

Inhibition of insulin release by CCB

48
Q

Atropine can be used

A

Bradyarrythmia

49
Q

Antidote for CCB toxicity

A

Calcium chloride or calcium gluconate(improves depression of cardiac contractility)/High dose insulin euglycemic therapy/cardiogenic shock -Epinephrine, Dobutamine, isoproterenol/vasodilatory shock -Norpinephrine and phenylephrine

50
Q

BAB action

A

Reduce CMV,Prolon diastole,Reduce AV conduction

51
Q

Use of BAB

A

Prevention of angina attack, antihypertensive

52
Q

SE of BAB

A

Bradycardia,AV block, Bronchospasm, cold extremities

53
Q

Nitrate action

A

Increase HR and contractility and decrease Arterial pressure,EDV, ejection time

54
Q

BAB and calcium channel blockers action

A

Increase ejection time and EDV, decrease HR, contractility,arterial pressure

55
Q

If NO combined with calcium channel blockers or BAB cause

A

Decrease in HR and Arterial pressure.No change in others

56
Q

Ivabradine acts on —–channel and Inhibits —-

A

HCN,Na ion flow in 4th phase of AP in SA node

57
Q

Ivabradine only cause decrease in

A

HR,not change contractility or induce vasoconstriction

58
Q

Use of ivabradin

A

Prevention of stable angina attack

59
Q

BAB is used only when

A

There is BAB intolerance or contraindications,as well as in combination

60
Q

SE of ivabradin

A

Light phenomenon in the retina (photopsy), pronounced bradycardia

61
Q

Ischemia induces accumulation of

A

Na and calcium ions in myocardium

62
Q

Ranolazine

A

Blocks na channel, indirectly reduce intracellular calcium ions,so decrease myocardial tension-decresed oxygen consumption and improve perfusion

63
Q

Ranolazine reduces the use of

A

GTN

64
Q

Atorvastatin action

A

Inhibition of HMG co A reductase+pleiotropic effects, decrease synthesis of mevalonic acid in liver, Increase LDL receptor and decrease LDL in plasma

65
Q

Atorvastatin uses

A

Dyslipidemia and prevention of cardiovascular events

66
Q

SE of atorvastatin

A

Hepatic function impairment (hepatopathy), myopathy

67
Q

Fenofibrate are

A

Fibric acid derivatives or PPAR alpha agonist

68
Q

Activation of PPAR alpha leads to activation of

A

Serum lipoprotein lipase -lipolysis-decrease TG and increase LDL receptor

69
Q

PPAR receptor are seen in

A

Blood vessel endothelium

70
Q

Cholesterol absorption inhibitor is

A

Ezetimibe

71
Q

Ezetimibe reduce the

A

Absorption of cholesterol in enterocyte villi by blocking NPC1L1 transport protein,It doesn’t affect fat soluble vitamins,bile acids,TG

72
Q

Evolozumab

A

PCSK9 inhibitor,inhibits LDL receptor degrading enzymes

73
Q

Evolozumab use —-to bond to PCSK9

A

Human IgG2 monoclonal antibody

74
Q

INOCA (vasospastic angina treatment

A

Calcium channel blockers,long acting organic nitrates

75
Q

Treatment for microvascular angina with structural changes

A

BAB,ACE inhibitors,Statins

76
Q

Treatment for microvascular angina vasospastic (functional form)

A

CCB,Long acting organic nitrates

Pharma 2 (7 decks)

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