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SRNAPharmacology I > Antiplatelets > Flashcards

Antiplatelets Flashcards

1
Q

know

A

durg, classificaiton, MOA, Epidural implications

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2
Q

Thienopyridine P2Y12 ADP-Receptor Antagonists

A
  • Ticlopidine (Ticlid®)
  • Clopidogrel (Plavix®)
  • Prasugrel (Effient®)
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3
Q

• Non-Thienopyridine P2Y12 ADP-Receptor Antagonists)

A
  • Ticagrelor (Brilinta®)

* Cangrelor (Kengreal®

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4
Q

• Glycoprotein IIb/IIIa Receptor Inhibitors/Antagonists

A
  • Abciximab (Reopro®)
  • Eptifibatide (Integrilin®)
  • Tirofiban (Aggrastat®)
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5
Q

ASA Mechanism of action

A

inhibits platelet aggregation by irreversible inhibition of platelet cyclooxygenase-1 (COX-1) enzyme, thereby preventing the formation of thromboxane A2, which is a potent platelet aggregate and potent vasoconstrictor

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6
Q

The effects of preventing platelet aggregation last for the

lifetime of the platelet

A

(7-10 days) since ASA produces irreversible inhibition of platelet cyclooxygenase-1

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7
Q

Aspirin absorption

•

A

Rapidly absorbed in stomach & upper intestine

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8
Q

• Rapidly cleared from the body (t1/2 =______) but the effects of aspirin on platelets are irreversible and last for the life of the

A

20 min; platelet (7-10 days)

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9
Q

Non-enteric coated plasma levels peak 30 to 40 minutes

A

Inhibition of platelet function occurs within 1 hour

• Enteric coated plasma levels peak 3 - 4 hours

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10
Q

ASA should be stop about

A

7-10 days

in general you dont have to

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11
Q

Dipyridamole

• Is both_____and _________

A

a vasodilator and antiplatelet agent

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12
Q

Mechanism of action of dipyridamole (1)

A
  1. Dipyridamole inhibits cyclic nucleotide phosphodiesterases, the enzyme that degrades cyclic adenosine monophosphate to 5′-AMP, resulting in the intraplatelet accumulation of cyclic AMP, which
    inhibits platelet aggregation
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13
Q

Mechanism of action of dipyridamole (2)

A
  1. Dipyridamole inhibits the uptake of adenosine into platelets and endothelial cells, which results in an increase in local adenosine concentrations that acts on platelet adenosine A2 receptors thereby stimulating platelet adenylyl cyclase which increases platelet cAMP
    levels & cAMP inhibits platelet aggregation
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14
Q

cyclic aMP tells platelets

A

non-adhere

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15
Q

Stop dipyridamole

A

• Discontinue 24 hours prior to surgery

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16
Q

Ticlopidine (Ticlid®)

A

• Thienopyridine Class Antiplatelet Agent

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17
Q

Ticlopidine (Ticlid®)

• Mechanism of action

A

The active metabolite then binds irreversibly to P2Y12 receptors on the surface of platelets and inhibits ADP induced platelet aggregation and activation
• Inhibits platelet function for the life span of the platelet (7-10 days)

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18
Q

Ticlid

A

• Is a prodrug that requires the liver for metabolic

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19
Q

KNOw FOR BOARDS • Hold 10 days prior to surgery and hold 14 days prior to placement of neuraxial anesthesia

A

KNonw for boards

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20
Q

Clinical use has all but been eliminated due to newer agents and due to ticlopidine’s risk of ____

A

causing severe neutropenia (ANC <

500/µL) and thrombotic thrombocytopenia purpuria (TTP)

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21
Q

Thienopyridine Class Antiplatelet Agent one agent

A

Clopidogrel

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22
Q

Mechanism of action of Clopidogrel

A

Is a prodrug that requires several liver CYP 450 enzymes for a 2-step metabolic conversion into its active metabolite. The active metabolite then binds irreversibly to P2Y12 receptors on the surface of platelets and inhibits ADP induced platelet aggregation and activation

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23
Q

Clopidogrel –>Inhibits platelet function for the life span of the platelet_______

A

(7-10 days)

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24
Q

For clopidogrel: Concomitant use of drugs that inhibit the CYP 450 enzymes used to metabolize clopidogrel to its active metabolite results in_______ plasma concentrations of the active metabolite of clopidogrel and a reduction in platelet inhibition

A

reduced

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25
Q

Clopidogrel, stop -_______ piror to surgery or elective surgery

A

7 days

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26
Q

Prasugrel (effient)

A

Is a more potent inhibitor of platelet aggregation than
clopidogrel and achieves more consistent and complete
inhibition of ADP-induced platelet aggregation. The trade off for this potent inhibition is a greater risk of bleeding from prasugrel compared to clopidogrel!

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27
Q

**Contraindications for PRASUGREL (EFFIENT)

A

• Any previous TIA or stroke (higher mortality)

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28
Q

Prasugrel

A

Discontinue at least 7 days prior to ANY surgery

29
Q

Ticagrelor is

A

• Non-thienopyridine class antiplatelet agent

30
Q

• Ticagrelor and its active metabolite bind

A

REVERSIBLY to P2Y12 receptors on the surface of platelets and inhibit ADP induced platelet aggregation and activation

31
Q

• Ticagrelor and its active metabolite are approximately

A

equipotent

32
Q

• Ticagrelor is not a prodrug and ________require metabolic activation –

A

DOES NOT

33
Q

Discontinue ticagrelor how many days prior to surgery

A

5 days before

34
Q

Contraindicated while epidural

catheter in place hold time before placement

A

Ticlopidine 14 dyas
Clopidogrel 7 days
Prasugrel 7 days
Ticagrelor 7 days

35
Q

kengreal (Cangrelor ) used as an

A

Used as an adjunct to PCI in the management of ACS patients

36
Q

Mechanism of action of Cangrelor

A

• Cangrelor is a direct P2Y12 platelet receptor inhibitor that blocks ADP-induced platelet activation and aggregation.
Cangrelor binds selectively and reversibly to the P2Y12
receptor to prevent further signaling and platelet activation

37
Q

Immediate onset and rapid offset______(medication) how soon does it take for platelet function to return to normal?

A

Cangrelor

Platelet functions return to normal in 60 minutes

38
Q

• Metabolism of Cangrelor

A

• Cangrelor is deactivated rapidly in the circulation by

dephosphorylation to its primary metabolite, a nucleoside

39
Q

Half life of Cangrelor

A

3-6 minutes

40
Q

No consideration for _____and ______in patients receiving cangrelor

A

liver and kidney

41
Q

**Vorapaxar (Zontivity®)

A

**protease-activated receptor 1 (PAR-1) antagonist/inhibitor

42
Q

**Vorapaxar (Zontivity®) Mechanism of action

A

Vorapaxar is a competitive, protease-activated receptor 1 (PAR-1) antagonist that inhibits thrombin-induced and
thrombin receptor agonist peptide (TRAP)-induced platelet aggregation

43
Q

Antiplatelet Agents: Glycoprotein IIb/IIIa

Antagonists Available in United States

A

Abciximab (Reopro®)
• Eptifibatide (Integrilin®)
• Tirofiban (Aggrastat®)

All have different MOA

44
Q

GIIb/IIIa antagonists Mechanism of action

A

bind competitively (reversibly) to the GP IIb/IIIa receptor on platelets and prevent the binding of fibrinogen, von Willebrand factor, and/ or other adhesive ligands to the GP IIb/IIIa receptor and thus inhibit platelet aggregation

45
Q

If patients on GIIb/IIIA they cannot

A

cannot go to surgery/epidural catheter

46
Q

Only us Giib/IIIa

A

as continuous IV

47
Q

Glycoprotein IIb/IIIa Antagonists:
Surgical Implications
• Abciximab
Typically discontinued__________

A

72 hours before surgery

48
Q
  • Eptifibitide and Tirofiban

* Typically discontinued

A

24 hours before surgery

49
Q

Can cause bleeding

A

GIIb/GIIIa

50
Q

hold time before placement

A

Abciximab 48 hours
EptifibatideΨ 4-8 hours
TirofibanΨ 4-8 hours

51
Q

Fibrinolytic agents

A

• These agents are called fibrinolytic or thrombolytic agents because they act as plasminogen activators since they convert endogenous proenzyme plasminogen into the fibrinolytic enzyme plasmin and plasmin then degrades fibrin into fibrin split products

52
Q

____is a major structural component of a thrombus

A

Fibrin

53
Q

Fibrin-specific agents

A

• These agents act preferentially on plasminogen molecules that are located within a fibrin clot and produce limited conversion of plasminogen into plasmin in the absence of fibrin, thus causing a limited systemic effect
• This fibrin specificity decreases systemic activation of
plasminogen and the resulting degradation of circulating
fibrinogen

54
Q

Plasminogen

A

can be free or bound to a clot

55
Q

Non-Fibrin-Specific Agents (aka: First generation agents)

•

A

Streptokinase (Streptase®) – No longer available in the U.S.A
• Urokinase (Abbokinase®) – No longer available in the U.S.A

56
Q

Fibrin-Specific Agents (aka: Second generation agents)

A
  • Alteplase (Activase®, Cathflo®Activase®)
  • Reteplase (Retavase®)
  • Tenecteplase (TNKase®)
57
Q

**Fibrinolytic/Thrombolytic Agents
Absolute contraindications
CASKAKI

A

Any prior intracranial hemorrhage/hemorrhagic stroke

  • Ischemic stroke within 3 months
  • Known structural cerebral vascular lesion
  • Arteriovenous malformation, Aneurysm
  • Known intracranial neoplasm
  • Suspected aortic dissection
  • Active Internal bleeding or bleeding diathesis
  • Considerable facial trauma or closed head trauma in past 3 months
58
Q

Fibrinolytic/thrombolytics

A

Relative contraindications
• Severe hypertension (SBP >180 and/or DBP >110)
• History of chronic poorly controlled hypertension
• INR 2-3 on warfarin
• Recent trauma, major surgery, prolonged CPR, minor head trauma,
internal bleeding within past 2-4 weeks
• Active peptic ulcer disease
• Streptokinase exposure > 5 days earlier or prior allergic reaction to streptokinase
• Pregnancy
• Age > 75 years
• Known intracranial pathology (dementia)

59
Q

• Streptokinase is a

A

non-enzymatic fibrinolytic agent produced by beta-hemolytic streptococci

60
Q

Streptokinase Mechanism of action

A

Rather, streptokinase binds non-covalently
to plasminogen (or binds to plasmin) to form a
streptokinase:plasminogen activator complex, and THIS
COMPLEX then acts on other plasminogen molecules to
generate plasmin

It binds to Plasminogen

61
Q

Plasmin

A

plasmin bind to plasmin split products and break down clot

62
Q

****Pharmacologic Properties of Fibrin-Specific
Thrombolytics
• Mechanism of action
• All available fibrin-specific thrombolytic agents have the same general mechanism of fibrinolysis

A

****• When introduced into systemic circulation, alteplase, reteplase, and tenectaplase preferentially bind to fibrin within a thrombus and enzymatically convert the entrapped plasminogen to plasmin. This initiates local fibrinolysis with limited systemic proteolysis. Plasmin breaks down fibrin into fibrin-split products. Fibrinogen, a
precursor to fibrin, is also degraded by plasmin
• They produce limited conversion of plasminogen in the absence of fibrin

63
Q

Alteplase (Activase®)

A

• Is a serine protease that acts as a tissue plasminogen activator and is manufactured by recombinant DNA technology

64
Q

Chemically identical to endogenous tPA

A

Alteplase

65
Q

• Plasma t1/2 = rt-PA

A

< 5 min (shorter than streptokinase)

66
Q

_____ metabolism is the major clearance mechanism for rt-PA

A

Liver

67
Q

only medication arpproved for Ischemic stroke

A

Alteplase

68
Q

rt-PA administration

A
  • Administer within 3 hours of stroke symptom onset
  • It is also appropriate to use within 3 to 4.5 hour window (there are additional inclusion criteria than 3 hour criteria)
69
Q

Catheter placement

A

NOOOO

SRNAPharmacology I (29 decks)

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