Antithrombotics Flashcards

1
Q

Primary hemostasis steps

A

Platelet shape change and activation
Platelet adhesion
Platelet aggregation

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2
Q

Secondary hemostasis step

A

Activation of intrinsic/extrinsic coagulation cascades

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3
Q

ADP activates platelets through a G_ protein coupled receptor

A

Gi

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4
Q

Anti platelet drugs

A

Aspirin
Clopidogrel
Abciximab
Vorapaxar

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5
Q

Thrombolytic drug

A

T-PA

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6
Q

Vitamin K antagonist

A

Warfarin

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7
Q

ADP receptor antagonist

A

Clopidogrel

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8
Q

Clopidogrel MOA

A

Prodrug metabolized in liver
Blocks platelet aggregation by binding irreversibly to P2Y12 ADP receptors

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9
Q

Clinical uses of clopidogrel

A

Reduce rate of stroke, MI, atherosclerosis
Similar but slightly.,more effective than aspirin

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10
Q

Black box warning for clopidogrel

A

Therapeutic failure in patients with loss of CYP2C19*2 allele
(Need to be tested for allele before starting drug)

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11
Q

Adverse effects of Clopidogrel

A

Bleeding
GI upset
Thrombotic thrombocytic purpura

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12
Q

Drug interactions with Clopidogrel

A

NSAIDs
omeprazole

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13
Q

Abciximab MOA

A

GPIIb/IIIa antagonist
Blocks platelet aggregation/fibrinogen binding

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14
Q

Clinical use of abciximab

A

Most effective anti platelet drug (very expensive)
Short term to prevent ischemic events

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15
Q

Vorapaxar MOA

A

Blocks PAR-1 receptor

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16
Q

Vorapaxar clinical use

A

Reduce thrombosis post-MI

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17
Q

How long does Vorapaxar effect last?

A

Up to 4 weeks

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18
Q

Boxed warning of vorapaxar

A

Bleeding (intracranial hemorrhage)

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19
Q

Antiplatelet drugs are effective against arterial/venous thrombi

A

Arterial

20
Q

Anticoagulants are effective against arterial/venous thrombi

A

Venous

21
Q

PTT is used to monitor intrinsic/extrinsic pathway anticoagulants

A

Intrinsic

22
Q

PT is used to monitor intrinsic/extrinsic pathway anticoagulants

A

Extrinsic

23
Q

Heparin inactivates ____ and ___ equally

A

Thrombin, Xa

24
Q

LMWh inactivates ___ well and ___ poorly

A

Xa, thrombin

25
Q

____ inactivates factor Xa only

A

Fondaparinux

26
Q

LMW heparin drugs

A

Enoxaparin
Fondaparinux

27
Q

MOA of heparins

A

Blocks formation of fibrin

28
Q

Heparin has no intrinsic/extrinsic activity

A

Intrinsic

29
Q

Clinical uses of heparin

A

Initial treatment of DVT/PE
Surgeries to prevent thrombosis

30
Q

Heparin antidote

A

Protamine sulfate (doesn’t work against fondaparinux)

31
Q

Heparin black box warning

A

Derived from pigs (cultural and allergic cautions)

32
Q

Vitamin K antagonist prototype

A

Warfarin

33
Q

MOA of vitamin K antagonists

A

Decreases vitamin K-dependent clotting factors by inhibiting VKORC1 in liver
Decreases formation of fibrin

34
Q

Vitamin K antagonists have slower/faster onset than heparin

A

Slower (takes several days for full effect vs 5 minutes for heparin; heparin used until warfarin takes effect)

35
Q

Patients on warfarin should be advised to avoid excess ___ in their diet

A

Vitamin K (leafy greens, fish, alcohol)

36
Q

Warfarin depletes endogenous anticoagulants, causing an initial _____ state

A

Hyper-coagulable

37
Q

Route of administration for warfarin

A

Oral

38
Q

Warfarin is ___% albumin bound

A

99%

39
Q

Warfarin therapy requires close monitoring via ___

A

PT/INR

40
Q

Warfarin is metabolized by which enzyme?

A

CYP2C9

41
Q

Clinical use of warfarin

A

Long-term prophylaxis of venous thrombosis

42
Q

Adverse effects of warfarin

A

Bleeding
Teratogen
Tissue necrosis
Purple toe syndrome

43
Q

Warfarin antidote

A

Vitamin K (phytonadione)

44
Q

Direct thrombin inhibitor drugs

A

Bivalirudin
Dabigatran etexilate

45
Q

Dabigatran advantage over warfarin

A

Don’t need to monitor INR

46
Q

Dabigatran antidote

A

Idarucizumab

47
Q

t-PA MOA

A

Converts plasminogen to plasmin that digests fibrin