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Pharmacology II Exam 2 (Lauren) > Coagulation Drugs Based On Review > Flashcards

Coagulation Drugs Based On Review Flashcards

1
Q

What happens when Factor X is activated?

A

Prothrombin is turned into Thrombin

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2
Q

Which pathways does heparin affect?

A

Intrinsic and common

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3
Q

Which natural inhibitor is heparin most dependent on?

A

Antithrombin III

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4
Q

Which factors are most affected by heparin

A

Xa and thrombin

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5
Q

What is the only route of administration for HMW heparin? Why?

A

IV only. It is a very big molecule (reason its called High molecular weight)

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6
Q

What will happen if you inject HMW heparin IM?

A

Hematoma

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7
Q

How long does it take for heparin to work?

A

Immediate

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8
Q

What are the adverse effects of heparin

A

Hemorrhage

Heparin induced Thrombocytopenia (HIT)

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9
Q

Who should NOT get heparin

A

During surgery of brain, spinal cord, or eyes=closed spaces. Excess bleeding= major damage

Active bleeds

Hemophilia

Hypersensitive

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10
Q

What are the other two drugs similar to HMW Heparin?

A

Enoxaprin- low-molecular weight heparin

Fondaparinux- synthetic pentasaccharide

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11
Q

Can enoxaprin and fondaparinux be given Subcutaneously?

A

Yes thank god

Especially since they are used to replace warfarin in pregnancy- sure would suck to have an IV for your whole pregnancy

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12
Q

What is the reversal agent for Heparin?

A

Protamine (works right away)

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13
Q

Does protamine work to reverse enoxaprin and Fondaparinux?

A

Enoxaprin- partially

Fondaparinux- NO effect

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14
Q

What does bivalirudin do?

A

Direct thrombin inhibitor (alternative to heparin if it caused HIT)

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15
Q

Where does bivalirudin come from?

A

leeches

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16
Q

Is Argatroban a direct inhibitor of factor Xa like Rivaroxaban, Apixaban, Edoxaban, and Betrixaban?

A

No. It is a direct inhibitor of thrombin. Tro(m) Ban sound like thrombin idk

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17
Q

Does protamine work for anything other than HMW and LMW heparin

A

No

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18
Q

What is the MOA of dabigatran (Pradaxa)

A

It is a direct thrombin inhibitor

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19
Q

Is Pradaxa monitored?

A

No it has predictable anticoagulant effects

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20
Q

What is the black box warning for Pradaxa

A

Avoid abrupt discontinuation = big risk of thrombotic events

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21
Q

How do you reverse dabigatran (pradaxa)

A

Idarucizumab (Praxbind)

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22
Q

What is the MOA for Rivaroxaban, Apixaban, Edoxaban, and Betrixaban?

A

Direct inhibitors of Xa

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23
Q

What is the route of administration of Rivaroxaban, Apixaban, Edoxaban, and Betrixaban?

A

ORAL

24
Q

How do you reverse Rivaroxaban, Apixaban, Edoxaban, and Betrixaban?

A

Andexxa (Factor Xa decoy)

25
Q

How do we measure the effects of Rivaroxaban, Apixaban, Edoxaban, and Betrixaban?

A

You dont. The effect is dose-dependent. (No PT/INR monitoring etc)

26
Q

What is the MOA of warfarin

A

Inhibits the reduction of vitamin K and interferes with the synthesis of II, VII, IX, and X (as well as protein C and S)

27
Q

What factors are effected by warfarin?

A

II, VII, IX, X****

28
Q

How long does it take for warfarin to work? Why?

A

4-5 days.

There will still be factors floating around that were synthesized before you started taking warfarin

29
Q

How do you need to start warfarin? Why?

A

Coadministered with Heparin for a few days because it will kill Protein C and S way before the clotting factors, and you will be MORE prone to clots for a few days

30
Q

Why does warfarin have so many drug interactions?

A

98% bound to proteins (any change in this status could be dangerous)

CYP450 metabolism

31
Q

What drugs affect warfarin

A

Antibiotics (kill the bacteria making your vitamin K)

Estrogen (combined oral contraceptives. Estrogen increases production of clotting factors)

Aspirin

32
Q

How do you reverse warfarin

A

Vitamin K (takes time)

Fresh frozen plasma (immediate)

33
Q

You have a clot. Can you give some heparin, warfarin, pradaxa, etc?

A

No. They have NO effect on already formed clots.

Need a thrombolytic drug

34
Q

What is the MOA of Alteplase (tPA) and Tenecteplase?

A

Convert plasminogen to plasmin

35
Q

What is another name for Alteplase

A

Tissue plasminogen activator or t-PA

36
Q

What are the 3 thrombolytics that are still on the market?

A

Alteplase (tPA)

Tenecteplase

Urokinase

37
Q

What makes Tenectaplase special?

A

It is CLOT SELECTIVE

Higher activity for fibrin-bound plasminogen vs plasma plasminogen

38
Q

What is the MOA of Urokinase?

A

Directly activates plasminogen

39
Q

Is urokinase clot-specific

A

No

40
Q

What are the 2 thrombolytics that are off the market

A

Streptokinase

Anistreplase

41
Q

You gave your patient some tPA for their DVT and Wooooops now they’re bleeding out. What do you do?

A

Administer aminocaproic acid or Tranexamic acid

These will inhibit plasminogen activation

42
Q

Wanna see a list of drugs that are antiPLATELETS not anticoagulants

A

Aspirin

Clopidigrel

Ticlopidine

Prasugrel

Abciximab

Eptfibatide

Tirofiban

Vorapaxar

43
Q

How does aspirin prevent platelet aggregation?

A

Irreversibly inhibits COX enzyme = no thromboxane/prostaglandin synthesis= no platelet aggregation

44
Q

How does the half life of aspirin compare to the duration of its effects

A

Effects last much longer than half life. Due to the irreversible inhibition of COX, effects will last the life of the platelet (7-10 days)

45
Q

How do clopidigrel, ticlopidine, and prasugrel inhibit platelet aggregation?

A

Irreversibly blocks the ADP receptor

46
Q

What drug will make clopidigrel not work?

A

Omeprazole- impairs CYP2C19 and will prevent activation of clopidigrel=clots

47
Q

Which antiplatelt drugs inhibit the GPIIb/IIIa receptor?

A

Abciximab

Eptifabatide

Tirofiban

48
Q

How are Apciximab, Eptifibatide, and Tirofiban administered?

A

IV only usually during percutaneous coronary intervention procedures (angioplasty, stenting, etc)

49
Q

What does varapaxar do?

A

Antagonist of the PAR-1 receptor on platelets (the major thrombin receptor on platelets)= inhibits platelet aggregation

50
Q

Argatroban and Dabigatran (Pradaxa) are both _______________.
The difference between them is that:

A

Direct thrombin inhibitors

Argatroban is IV

Dabigatran (Pradaxa) is oral

51
Q

Which direct factor Xa inhibitors are used the most, and which are used the least

A

Rivaroxaban and Apixaban: used most (been on market for a long time)

Edoxaban and Betrixaban: used for special cases (non valvular afib or critically ill)

52
Q

What is plasmin?

A

It is the active fibrinolytic enzyme

53
Q

In patients with established heart disease, can aspirin be used as a PRIMARY prevention of cardiovascular events?

A

No. Used as secondary prevention.

54
Q

What is the DOC to prevent thrombosis in patients undergoing placement of stents?

A

Clopidigrel, Ticlopidine, Prasugrel

ADP receptor blockers

55
Q

What are abciximab, eptifibatide, and tirofiban (the GP IIb/IIIa inhibitors) used for?

A

They are combined with heparin and given during percutaneous coronary intervention like angioplasty, atherectomy, and stent placement

Pharmacology II Exam 2 (Lauren) (9 decks)

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