Coagulation Drugs Based On Review

Question 1

What happens when Factor X is activated?

Answer 1

Prothrombin is turned into Thrombin

Question 2

Which pathways does heparin affect?

Answer 2

Intrinsic and common

Question 3

Which natural inhibitor is heparin most dependent on?

Answer 3

Antithrombin III

Question 4

Which factors are most affected by heparin

Answer 4

Xa and thrombin

Question 5

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

Answer 5

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

Question 6

What will happen if you inject HMW heparin IM?

Answer 6

Hematoma

Question 7

How long does it take for heparin to work?

Answer 7

Immediate

Question 8

What are the adverse effects of heparin

Answer 8

Hemorrhage

Heparin induced Thrombocytopenia (HIT)

Question 9

Who should NOT get heparin

Answer 9

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

Active bleeds

Hemophilia

Hypersensitive

Question 10

What are the other two drugs similar to HMW Heparin?

Answer 10

Enoxaprin- low-molecular weight heparin

Fondaparinux- synthetic pentasaccharide

Question 11

Can enoxaprin and fondaparinux be given Subcutaneously?

Answer 11

Yes thank god

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

Question 12

What is the reversal agent for Heparin?

Answer 12

Protamine (works right away)

Question 13

Does protamine work to reverse enoxaprin and Fondaparinux?

Answer 13

Enoxaprin- partially

Fondaparinux- NO effect

Question 14

What does bivalirudin do?

Answer 14

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

Question 15

Where does bivalirudin come from?

Answer 15

leeches

Question 16

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

Answer 16

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

Question 17

Does protamine work for anything other than HMW and LMW heparin

Answer 17

No

Question 18

What is the MOA of dabigatran (Pradaxa)

Answer 18

It is a direct thrombin inhibitor

Question 19

Is Pradaxa monitored?

Answer 19

No it has predictable anticoagulant effects

Question 20

What is the black box warning for Pradaxa

Answer 20

Avoid abrupt discontinuation = big risk of thrombotic events

Question 21

How do you reverse dabigatran (pradaxa)

Answer 21

Idarucizumab (Praxbind)

Question 22

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

Answer 22

Direct inhibitors of Xa

Question 23

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

Answer 23

ORAL

Question 24

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

Answer 24

Andexxa (Factor Xa decoy)

Question 25

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

Answer 25

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

Question 26

What is the MOA of warfarin

Answer 26

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

Question 27

What factors are effected by warfarin?

Answer 27

II, VII, IX, X**************

Question 28

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

Answer 28

4-5 days. There will still be factors floating around that were synthesized before you started taking warfarin

Question 29

How do you need to start warfarin? Why?

Answer 29

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

Question 30

Why does warfarin have so many drug interactions?

Answer 30

98% bound to proteins (any change in this status could be dangerous) CYP450 metabolism

Question 31

What drugs affect warfarin

Answer 31

Antibiotics (kill the bacteria making your vitamin K) Estrogen (combined oral contraceptives. Estrogen increases production of clotting factors) Aspirin

Question 32

How do you reverse warfarin

Answer 32

Vitamin K (takes time) Fresh frozen plasma (immediate)

Question 33

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

Answer 33

No. They have NO effect on already formed clots. Need a thrombolytic drug

Question 34

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

Answer 34

Convert plasminogen to plasmin

Question 35

What is another name for Alteplase

Answer 35

Tissue plasminogen activator or t-PA

Question 36

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

Answer 36

Alteplase (tPA) Tenecteplase Urokinase

Question 37

What makes Tenectaplase special?

Answer 37

It is CLOT SELECTIVE | Higher activity for fibrin-bound plasminogen vs plasma plasminogen

Question 38

What is the MOA of Urokinase?

Answer 38

Directly activates plasminogen

Question 39

Is urokinase clot-specific

Answer 39

No

Question 40

What are the 2 thrombolytics that are off the market

Answer 40

Streptokinase Anistreplase

Question 41

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

Answer 41

Administer aminocaproic acid or Tranexamic acid These will inhibit plasminogen activation

Question 42

Wanna see a list of drugs that are antiPLATELETS not anticoagulants

Answer 42

Aspirin Clopidigrel Ticlopidine Prasugrel Abciximab Eptfibatide Tirofiban Vorapaxar

Question 43

How does aspirin prevent platelet aggregation?

Answer 43

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

Question 44

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

Answer 44

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)

Question 45

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

Answer 45

Irreversibly blocks the ADP receptor

Question 46

What drug will make clopidigrel not work?

Answer 46

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

Question 47

Which antiplatelt drugs inhibit the GPIIb/IIIa receptor?

Answer 47

Abciximab Eptifabatide Tirofiban

Question 48

How are Apciximab, Eptifibatide, and Tirofiban administered?

Answer 48

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

Question 49

What does varapaxar do?

Answer 49

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

Question 50

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

Answer 50

Direct thrombin inhibitors Argatroban is IV Dabigatran (Pradaxa) is oral

Question 51

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

Answer 51

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)

Question 52

What is plasmin?

Answer 52

It is the active fibrinolytic enzyme

Question 53

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

Answer 53

No. Used as secondary prevention.

Question 54

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

Answer 54

Clopidigrel, Ticlopidine, Prasugrel | ADP receptor blockers

Question 55

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

Answer 55

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