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CPR II Week 2 > Drugs Used in ACS/Stable Angina > Flashcards

Drugs Used in ACS/Stable Angina Flashcards

1
Q

What is stable angina?

When do symptoms occur?

A

1) Occlusion of coronary arteries resulting from the formation of atherosclerotic plaque
2) During exertion or stress

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2
Q

What is Vasospastic angina?

When do symptoms occur?

A

1) Episodes of vasoconstriction of coronary arteries

2) At rest

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3
Q

What are the two approaches to treat stable angina?

A

1) To increase (or restore) coronary blood flow

2) To reduce myocardial oxygen demand

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4
Q

What pharmacotherapy regimen is used to increase blood flow through the stenotic coronary artery in order to treat stable angina?

A

There is none

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5
Q

What are the nitrates used in treating stable angina?

A

1) Nitroglycerin
2) Isosorbide dinitrate
3) Isosorbide mononitrate

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6
Q

Why do nitrates have a significant first-pass metabolism?

A

High nitrate reductase activity in the liver

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7
Q

What is the MOA of nitrates in stable angina?

A

Nitrates release NO which causes cGMP to activate protein kinase G causing venous dilation and reduced preload which ultimately leads to decrease in O2 demand

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8
Q

The development of tolerance to nitrates leads to the increased generation of?

A

Superoxide radical

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9
Q

Short-acting formulations of nitrates are used to?

Long-acting preparations may be used to?

A

1) Relieve the angina attack

2) Prevent attacks

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10
Q

What drug interaction are seen with nitrates?

What does it cause molecularly?

What conditions have been reported due to the interaction?

A

1) Drugs used in ED such as sildenafil, vardenafil, and tadalafil
2) Massive increase in cGMP
3) Acute MI

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11
Q

What are the non-cardioactive (dihydropyridines) calcium channel blockers used in treating stable angina?

A

1) Amlodipine
2) Nifedipine
3) Nicardipine

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12
Q

What are the cardioactive calcium channel blockers used in treating stable angina?

A

1) Diltiazem

2) Verapamil

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13
Q

The non-cardioactive calcium channel blockers act on?

A

Vascular smooth muscle

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14
Q

The cardioactive calcium channel blockers act on?

A

1) Vascular smooth muscle
2) Cardiac muscle
3) Cardiac pacemakers cells

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15
Q

What is the end goal of calcium channel blockers in order to treat stable angina?

A

Decrease myocardial O2 demand

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16
Q

How do calcium channel blockers decrease myocardial O2 demand?

(Indicate if the MOA is done by dihydropyridines or by cardioactive CCB)

A

1) Dilation of peripheral arterioles (Both)
2) Decrease cardiac contractility (Cardioactive CCB)
3) Reduce heart rate (Cardioactive CCB)

17
Q

What are the beta-blockers used in treatment of stable angina?

A

1) Propranolol
2) Nadolol
3) Metoprolol
4) Atenolol

18
Q

What is the end goal of beta-blockers in order to treat stable angina?

How does it accomplish this?

A

1) Decrease myocardial O2 demand

2) Decrease HR, cardiac contractility, and BP

19
Q

What is the MOA of ranolazine?

A

Inhibits late Na+ current in cardiomyocytes

20
Q

Ranolazine may reduce?

A

1) Diastolic tension and compression of coronary vessels in diastole
2) Cardiac contractility and oxygen demand

21
Q

What is the goal in treating vasospastic angina?

A

To relieve coronary spasm and increase blood flow into the affected area using vasodilators

22
Q

What are the first choice drugs for treating vasospastic angina?

A

CCBs such as Diltiazem or amlodipine

23
Q

If CCBs are contraindicated due to low BP, bradycardia, or AV block what are used instead to treat vasospastic angina?

A

Long-acting nitrates

24
Q

Where do red thrombus form?

What are they composed of?

What pathologic condition is it associated with?

A

1) In low-pressure veins and in the heart
2) Fibrin-rich with trapped RBCs
3) Embolic stroke

25
Q

Where do white thrombus form?

What are they composed of?

What pathologic condition is it associated with?

A

1) In high-pressure arteries
2) Platelet rich
3) Acute coronary syndrome

26
Q

What drug class is used to prevent white thrombi from forming in the arteries?

Prevent red thrombi from forming in venous system?

Re-establish blood flow through vessels once clots have formed?

A

1) Antiplatelet drugs
2) Anticoagulants
3) Thrombolysis

27
Q

What antiplatelet drug is an inhibitor of thromboxane A2 synthesis?

A

Aspirin

28
Q

Clopidogrel, Prasugrel, and Ticagrelor make up what class of antiplatelet drugs?

A

P2Y12 (ADP) Receptor Blockers

29
Q

Abciximab, Eptifibatide, and Tirofiban make up what class of antiplatelet drugs?

A

Platelet glycoprotein IIB/IIIA receptor blockers

30
Q

What is the MOA of aspirin?

A

Irreversible inhibition of cyclooxygenase to block TxA2 production

31
Q

What is the MOA of the P2Y12 (ADP) Receptor Blockers?

A

Blocks these receptors to increase adenylyl cyclase activity and cAMP levels which prevent platelet aggregation

32
Q

What populations have the highest resistance to clopidogrel?

Why?

A

1) Chinese and African Americans

2) CYP2C19 allele present

33
Q

What is the MOA of Abciximab, Eptifibatide, and Tirofiban?

A

Prevent binding of ligands to the GP IIb/IIIa receptor to inhibit platelet aggregation

34
Q

What is an adverse effect of the glycoprotein IIB/IIIA receptor blockers that is more often seen with abciximab?

A

Thrombocytopenia

35
Q

Alteplase, Reteplase, Tenecteplase are the thrombolytic drugs that fall under the category of?

What thrombolytic drug is in its own separate category?

A

1) Tissue-type Plasminogen Activator (tPA)

2) Streptokinase

36
Q

What do thrombolytic drugs induce?

How does it do this?

A

1) Fibrinolysis

2) Converting plasminogen into plasmin

37
Q

What clinical use do thrombolytic drugs have?

A

Used in STEMI within 12 hours

CPR II Week 2 (6 decks)

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