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Cardiovascular > SM 132 CAD Pharmacology > Flashcards

SM 132 CAD Pharmacology Flashcards

1
Q

What factors influence Oxygen demand?

A

Heart Rate, Contractility, Wall Tension

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2
Q

What pathway are Nitrates associated with?

A

Nitrates activate the cGMP pathway to cause vasorelaxation

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3
Q

What are Nitrates primarily used for?

A

Short term relief of acute chest pain

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4
Q

How do Nitrates work?

A

Nitrates cause VENOdilation, reducing myocardial wall tension and therefore reducing oxygen requirements

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5
Q

What are Direct Renin Inhibitors?

A

Block the first step in the activation of the renin-angiotensin pathway to treat congestive heart failure

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6
Q

What does platelet activation result in?

A

Expression of GP IIbIIIa receptor and a change in shapde

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7
Q

What are the low molecular weight heparins?

A

Enoxaparin and Dalteparin

Inhibit Factor Xa > Factor II

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8
Q

What factors can activate platelets?

A

Shear stress, ADP, Epinepthrine, Collagen, Thrombin

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9
Q

Which Beta Blocker has a long half life?

A

Nadolol

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10
Q

What is required for GP IIbIIIa expression, and what role does it mediate?

A

Platelet activation is required for GP IIbIIIa expression

GP IIbIIIa mediates binding to Fibrinogen

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11
Q

How do Aldosterone receptor antagonists work?

A

Block the interaction of Aldosterone with its receptor, leading to lower blood pressure and lower sodium retention

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12
Q

What class of drugs does Ticagrelor belong to?

A

Ticagrelor is a Triazolopyrimidine

NOT a Thienopyridine like Clopidogrel and Prasugrel

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13
Q

How do Thienopyridines work?

A

Inhibit P2Y12 ADP receptor mediated activation of platelets to reduce clot formation

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14
Q

Name an example of an Aldosterone receptor antagonist?

A

Spironolactone

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15
Q

What effect does increasing dose have on a Beta Blocker?

A

Higher doses of a Beta Blocker are less specific to Beta1 or Beta2 receptors

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16
Q

Why is Reocclusion a risk with fibrinolytic reperfusion?

A

Fibrinolytic reperfusion does nothing to address the causes of clot formation, and only breaks an existing clot, so another could reform later

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17
Q

What are the side effects of Beta Blockers?

A

Sedation and Asthma

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18
Q

What are Beta Blockers primarily used for?

A

Reduce mortality and reinfarction after MI

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19
Q

What are the advantages of Fibrinolytic reperfusion over surgical approaches?

A

Universally available
Ease of use
Rapid administration

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20
Q

What are the GP IIbIIIa inhibitors?

A

Abciximab, Tirofibin, Eptifibatide

Prevent platelet aggregation

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21
Q

How do Calcium Channel Blockers work?

A

Block Calcium channels in the vascular smooth muscle and myocardium resulting in improved myocardial blood flow and lower blood pressure

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22
Q

Which Beta Blocker is nonspecific?

A

Propranolol; blocks both Beta1 and Beta2 receptors

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23
Q

When are plasminogen activators used?

A

Rapid dissolution of a clot during STEMI

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24
Q

What factors influence Oxygen supply?

A

Coronary Blood Flow is set by Diastolic Time, Collateral supply, and the Aortic Diastole - LVEDP gradient

25
Q

How do ARB works?

A

Angiotensin Receptor Blockers prevent binding of Angiotensin II to the AT1 receptor, effecting the vasculature, heart, kidney, and muscle

Useful for Heart Failure, Left Ventricular Systolic Dysfunction, Hypertension

26
Q

How does Ticagrelor work?

A

Inhibits platelet activation via ADP receptor pathway

27
Q

How do plasminogen activators work?

A

They cleave Plasminogen into Plasmin and degrade the fibrin strands holding a thrombus together

28
Q

What are the plasminogen activators?

A

Streptokinase, Alteplase, and Tenecteplase

29
Q

What functions does ACE have other than the conversion of Angiotensin?

A

ACE inactivates Bradykinin and Enkephalins

ACE inhibitors potentiate Bradykinin and cause cough

30
Q

How do Beta Blockers work?

A

Beta Blockers lower HR and improve Diastolic Filling Time, lowering BP and preventing exercise induced increases in myocardial contractility

31
Q

What are the main side effects of Nitrates?

A

Headache and dizziness; rapid development of tolerance

32
Q

What gradient determines coronary perfusion?

A

The gradient between Aortic Diastolic Pressure and LVED determines the coronary perfusion

33
Q

How does Ranolazine work?

A

Ranolazine reduces the late inward Na current in ischemic myocardium, thereby lowering intracellular Na and restricting Na/Ca exchange, ultimately lowering contractility

34
Q

What is the most common side effect of Verapamil and Diltiazem?

A

Bradycarida and heart failure

35
Q

How do Triazolopyrimidines compare to Trhienopyridines?

A

Triazolopyrimidines are reversible, active drugs with rapid onset

Thienopyridines are irreversible, prodrugs with slow onset

Triazolopyrimidines include Ticagrelor

Thienopyridines include Clopidogrel and Prasugrel

Both Triazolopyrimidines and Thienopyridines effect P2Y12 receptors

36
Q

When is Warfarin the anticoagulative of choice?

A

OVAHP

Outpatient setting
Venous Thromboembolitic Disease
Heart Valves
Atrial Fibrillation
Prior Emboli
37
Q

What are the side effects of ARB?

A

Minimal

38
Q

What can Beta Blockers not improve?

A

Beta Blockers cannot improve Oxygen supply, only decrease Oxygen demand

39
Q

What is the suffix of ACE inhibitors?

A

-pril

40
Q

How do ACE inhibitors work?

A

ACE Inhibitors prevent the formation of Angiotensin II from Angiotensin I

Used for Hypertension, Heart Failure, MI

41
Q

What drugs fall in the Thienopyridine class?

A

Clopidogrel and Prasugrel

NOT Ticagrelor

42
Q

Name an example of a DIrect Renin Inhibitor?

A

Aliskiren

43
Q

What are the disadvantages of Fibrinolytic reperfusion over surgical approaches?

A

Hemorrhage/stroke risk
Reocclusion
Contraindications
~50-60% optimal flow restoration

44
Q

Why is Tenecteplase the best fibrinolytic agent?

A

Dosed as a single bolus, high fibrin specificity to a specific clot, directly activates Plasminogen and is not antigenic

45
Q

Why might a fibrinolytic reperfusion agent like Streptokinase cause ICH?

A

Intracranial hemorrhage can arise after an agent like Streptokinase is administered because healthy clots are broken as well, potentially leading to ICH

46
Q

What is the suffix of ARB drugs?

A

-artan

47
Q

How do Dihydropyridine and Non-dihydropyridine agents differ in their effects on heart rate?

A

Both are Calcium channel blockers

Dihydropyridines increase HR while Non-dihydropyridines decrease HR

48
Q

What are the side effects of ACE Inhibitors?

A

Nonproductive cough

49
Q

How does the GP IIbIIIa receptor affect platelet function?

A

Activation of the receptor allows platelets to tightly bind eachother, with Fibrinogen acting as the connection between two platelets

50
Q

What are the effects and outcomes of Calcium antagonists?

A

Calcium antagonists inhibit vasoconstriction and enhance ventricular relaxation

Decrease Oxygen demand and increase Oxygen supply

51
Q

How do small molecule GP IIbIIIa inhibitors compare to peptide inhibitors?

A

Small molecule inhibitors have a shorter half life and need continuous IV infusion

52
Q

How does the dose of aspirin determine it’s effects?

A

Low dose aspirin inhibits Thromboxane A2 synthesis, opposing clots

High dose aspirin inhibits Prostacyclin synthesis, promoting clots

53
Q

What are the Dihydropyridines?

A

Calcium Channel Blockers FANN

Felodipine
Amlodipine
Nifedipine
Nicardipine

All are arterial vasodilators

54
Q

What are GP IIbIIIa inhibitors used for?

A

Angioplasty and stenting

55
Q

Which Beta Blocker has anti alpha-adrenergic effects?

A

Carvedilol

56
Q

What are the effects and outcomes of Nitrates?

A

Nitrates cause vasodilation and decrease preload

Decrease Oxygen demand and improve Oxygen supply

57
Q

What are the side effects of Dihidropyridines?

A

Pedal edema

58
Q

What are the effects and outcomes of Beta Blockers?

A

Beta Blockers treat chronic angina by decreasing HR, contractility, and BP

Decrease Oxygen demand

Cardiovascular (25 decks)

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