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Cardio Exam 2 > Part 2 of Pharmacology for CAD and Stroke > Flashcards

Part 2 of Pharmacology for CAD and Stroke Flashcards

1
Q

ADP Receptor Blockers are also known as?

A

Thienopyridines

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2
Q

ADP is a

A

potent initiator of platelet aggregation via P2Y12 and P2Y1

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3
Q

P2Y12 and P2Y1 receptors

A

Have to both be stimulated in order for platelet activation to occur
So for drugs, all you have to do is block one to block platelet activation

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4
Q

Thienopyridines Examples

A

Prasugrel

Clopidgrel

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5
Q

Thienopyridines are

A

Prodrugs
Metabolites bind to P2Y12 for irreversible blockage
Short half lives by long lasting effects

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6
Q

Thienopyridines Use

A

During ACS esp with angioplasty and stenting

Secondary prevention of MI and atheroembolic stroke

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7
Q

Thienopyridines Important Considerations

A

Metabolism is required fo activity
Inhibition is irreversible
Nature of metabolizing enzyme is key for efficacy

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8
Q

Clopidegrel requires

A

2C19

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9
Q

Prasegrel requires

A

3A4

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10
Q

Slow metabolizers should use:

A

Prasegrel

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11
Q

Reversible ADP Receptor Antagonists is otherwise known as

A

A non-thienopyridine

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12
Q

Example of Non-thienopyridine

A

Ticagrelor

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13
Q

Ticagrelor is

A

NOT a pro-drug
Metabolized by 3A4
BID

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14
Q

Ticagrelor MOA

A

Reversible blockade of P2Y12 receptor with quick recovery after stopping the drug

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15
Q

Thrombin receptor antagonists otherwise known as:

A

Protease-activated receptor 1

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16
Q

Example of a Thrombin Receptor Antagonists

A

Vorapaxar (Zontivity)

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17
Q

Thrombin background

A

Causes platelet activation and aggregation through PAR 1/4

Most potent activator

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18
Q

PAR1 is

A

high affinity receptor (more sensitive)

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19
Q

Vorapaxar MOA

A

PAR1 has it’s ligand on it so thrombin comes in to activate it and then Vorapaxar binds the domain where the ligand would normally bind
Making it inactive

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20
Q

Aspirin blocks

A

formation of TXA2

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21
Q

Prasugrel and Clopidogrel block

A

ADP receptor

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22
Q

Vorapaxar Use

A

MI and PAD

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23
Q

Glycoprotein IIb/IIIa

A

Platelet surface protein
Receptor for fibrinogen and vWF
When activated it anchors platelets to each other via fibrinogen and to the surface via vWF

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24
Q

What activated Glycoprotein IIb/IIIa?

A

Thrombin, TXA2, ADP, Collagen

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25
Q

So why are glycoprotein IIb/IIIa inhibitors good?

A

Because the activators of the glycoprotein can still interact with their receptor but that won’t matter if the glycoprotein is inhibited

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26
Q

Glycoprotein IIb/IIIa inhibitors MOA

A

inhibit interaction of glycoprotein IIb/IIIa with fibrinogen and vWF to impair platelet aggregation

27
Q

Glycoprotein IIb/IIIa inhibitors Examples

A

Abciximab
Eptifibatide
Tirofiban

28
Q

Abciximab MOA

A

Binds to inactivated platelets to prevent coagulation

29
Q

Eptifibatide and Tirofiban MOA

A

Requires activated platelets and GP IIb/IIIa to bind and inhibit

30
Q

Abciximab Use

A

With angioplasty for coronary thromboses

With aspirin and heparin to prevent restenosis and MIs

31
Q

Eptifibatide and Tirofiban Use

A

UA, ACS, MI

Angioplastic coronary interventions

32
Q

***Absolute Contraindications for Glycoprotein IIb/IIIa inhibitors and Fibrinolytics

A 
Active internal bleed
Intracranial bleed
Intracranial tumor/aneurysm
Aortic dissection
Head/facial trauma (3 months)
Prior ischemic stroke (3 months)
33
Q

**Relative Contraindications for Glycoprotein IIb/IIIa inhibitors and Fibrinolytics

A 
Severe HTN not controlled by Rx
Dementia
Current use of warfarin
Bleeding diathesis
Active peptic ulcer
Prior ischemic stroke (more than 3 month)
Major surgery (3 wks)
Prior interal bleed (2-4 wks)
Traumatic or prolong CPR (more than 10 mins)
34
Q

Plasminogen –>

A

via tissue plasminogen activator makes plasmin which goes to enhance fibrinolysis (degradation of fibrin)

35
Q

Fibrinolytic agents examples

A

Alteplase
Reteplace
Tenecteplase

36
Q

Alteplase (Activase)

A

Shorter half-life

37
Q

Reteplase (Retavase)

Tenecteplase (TNKase)

A

Longer half life

38
Q

FIbrinolytic agent Use

A

acute MI and thromboembolic stroke

39
Q

Statins MOA

A

Blocks HMG-CoA reductase (conversion to mevalonic acid so no cholesterol)

40
Q

Beneficial effects of Statins

A

Lipid

Pleiotropic effects

41
Q

Main adverse effects of Statins

A

Myopathy
Cognitive effects
Hepatotoxicity
Hyperglycemia

42
Q

MOA of ACEi

A

Inhibit angiotensin converting enzyme which converts AngI to AngII so no renin production and Ang1-7 and bradykinin will be produced

43
Q

Main adverse effects of ACEi

A

Cough

Angioedema

44
Q

Pure anti-anginal agent example

A

Ranolazine (Ranexa)

45
Q

Ranolazine Use

A

Chronic angina

Combo with amlodipine, BB, or nitrate

46
Q

Ranolazine MOA

A

Not because of reduction of BP, HR or workload
Inhibit FA oxidation –> ATP is formed from glucose –> improved oxygen consumption
OR inhibit late sodium current and decrease calcium overload during ischemic attack

47
Q

Ranolazine + CYP

A

3A4 metabolized

48
Q

Main adverse effevts of Ranolazine

A

Constipation

Prolongation of QT interval

49
Q

CAUTION with Ranolazine

A

With diltiazem and verapamil bc of 3A4 inhibition

50
Q

Define stroke

A

Disease affecting blood vessels that supply blood to the brain

51
Q

Two types of stroke

A

Hemorrhagic (damage of vessels and bleeding)

Ischemic (blockage of a blood vessel by clot/mass

52
Q

Define Thrombus

A

Forms in a brain artery

53
Q

Define Embolus

A

Wandering clot

Formed away form the brain and comes and blocks the blood flow

54
Q

Ischemic and TE Stroke Therapeutic goals

A

Reduce neurologic injury
Decrease morality and long-term disability
Prevent complication secondary to immobility and dysfunction
Prevent stroke recurrence

55
Q

Acute Stroke Treatment

A

Fibrinolytics

Anti-platelets

56
Q

Fibrinolytics agents

A

Alteplase
Reteplase
Tenecteplase
Help restore perfusion

57
Q

Antiplatelet agents

A

Aspirin

Reduces aggregative activity of platelets

58
Q

Secondary prevention treatment

A

Anti-platelets

Anti-coagulants

59
Q

Anti-platelets

A

Used for atheroembolic stroke where platelets are a mjaor component of the thrombus

60
Q

Anticoagulants

A

Used for cardio/TE stroke where clotting factors are primary components of thrombus

61
Q

ACEi and Thiazides

A

BP Lowering agents
Beneficial independent of HTN
Reduce the risk of stroke recurrence
Not used in the first 7 days of acute stroke period

62
Q

ARBs

A

Alternative to ACEi

Cross BBB and may have more beneficial effects

63
Q

Statins

A

Reduce risk of stroke in pts with CAD and elevated lipids
in ALL ischemic stroke pts
Beneficial effect: lipid lower and pleiotropic effects

Cardio Exam 2 (10 decks)

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