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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
Clopidogrel, stop -_______ piror to surgery or elective surgery
7 days
26
Prasugrel (effient)
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!
27
****Contraindications for PRASUGREL (EFFIENT)
• Any previous TIA or stroke (higher mortality)
28
Prasugrel
Discontinue at least 7 days prior to ANY surgery
29
Ticagrelor is
• Non-thienopyridine class antiplatelet agent
30
• Ticagrelor and its active metabolite bind
REVERSIBLY to P2Y12 receptors on the surface of platelets and inhibit ADP induced platelet aggregation and activation
31
• Ticagrelor and its active metabolite are approximately
equipotent
32
• Ticagrelor is not a prodrug and ________require metabolic activation –
DOES NOT
33
Discontinue ticagrelor how many days prior to surgery
5 days before
34
Contraindicated while epidural | catheter in place hold time before placement
Ticlopidine 14 dyas Clopidogrel 7 days Prasugrel 7 days Ticagrelor 7 days
35
kengreal (Cangrelor ) used as an
Used as an adjunct to PCI in the management of ACS patients
36
Mechanism of action of Cangrelor
• 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
Immediate onset and rapid offset______(medication) how soon does it take for platelet function to return to normal?
Cangrelor | Platelet functions return to normal in 60 minutes
38
• Metabolism of Cangrelor
• Cangrelor is deactivated rapidly in the circulation by | dephosphorylation to its primary metabolite, a nucleoside
39
Half life of Cangrelor
3-6 minutes
40
No consideration for _____and ______in patients receiving cangrelor
liver and kidney
41
****Vorapaxar (Zontivity®)
****protease-activated receptor 1 (PAR-1) antagonist/inhibitor
42
****Vorapaxar (Zontivity®) Mechanism of action
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
Antiplatelet Agents: Glycoprotein IIb/IIIa | Antagonists Available in United States
Abciximab (Reopro®) • Eptifibatide (Integrilin®) • Tirofiban (Aggrastat®) All have different MOA
44
GIIb/IIIa antagonists Mechanism of action
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
If patients on GIIb/IIIA they cannot
cannot go to surgery/epidural catheter
46
Only us Giib/IIIa
as continuous IV
47
Glycoprotein IIb/IIIa Antagonists: Surgical Implications • Abciximab Typically discontinued__________
72 hours before surgery
48
* Eptifibitide and Tirofiban | * Typically discontinued
24 hours before surgery
49
Can cause bleeding
GIIb/GIIIa
50
hold time before placement
Abciximab 48 hours EptifibatideΨ 4-8 hours TirofibanΨ 4-8 hours
51
Fibrinolytic agents
• 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
____is a major structural component of a thrombus
Fibrin
53
Fibrin-specific agents
• 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
Plasminogen
can be free or bound to a clot
55
Non-Fibrin-Specific Agents (aka: First generation agents) | •
Streptokinase (Streptase®) – No longer available in the U.S.A • Urokinase (Abbokinase®) – No longer available in the U.S.A
56
Fibrin-Specific Agents (aka: Second generation agents)
* Alteplase (Activase®, Cathflo®Activase®) * Reteplase (Retavase®) * Tenecteplase (TNKase®)
57
****Fibrinolytic/Thrombolytic Agents Absolute contraindications CASKAKI
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
Fibrinolytic/thrombolytics
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
• Streptokinase is a
non-enzymatic fibrinolytic agent produced by beta-hemolytic streptococci
60
Streptokinase Mechanism of action
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
Plasmin
plasmin bind to plasmin split products and break down clot
62
******Pharmacologic Properties of Fibrin-Specific Thrombolytics • Mechanism of action • All available fibrin-specific thrombolytic agents have the same general mechanism of fibrinolysis
******• 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
Alteplase (Activase®)
• Is a serine protease that acts as a tissue plasminogen activator and is manufactured by recombinant DNA technology
64
Chemically identical to endogenous tPA
Alteplase
65
• Plasma t1/2 = rt-PA
< 5 min (shorter than streptokinase)
66
_____ metabolism is the major clearance mechanism for rt-PA
Liver
67
only medication arpproved for Ischemic stroke
Alteplase
68
rt-PA administration
* 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
Catheter placement
NOOOO

SRNAPharmacology I (29 decks)

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