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Heme > Clotting Pharm > Flashcards

Clotting Pharm Flashcards

1
Q

Function: Thromboxane A2

A

Platelet aggregation, Release response, Arterial constriction

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2
Q

Activates platelet aggregation

A

Thromboxane A2

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3
Q

Functions: Prostacyclin

A

Inhibit platelet aggregation, Relaxation of blood vessels

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4
Q

Inhibits platelet aggregation

A

Prostacyclin

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5
Q

Binds to the enzyme inhibitor antithrombin III (AT) causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop. The activated AT then inactivates thrombin and other proteases involved in blood clotting, most notably factor Xa. It can increase (by up to 1000-fold )the rate of inactivation of these proteases by AT

A

Unfractionated Heparin

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6
Q

MOA: Unfractionated Heparin

A

Inhibition of factor Xa and thrombin activity

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7
Q

Kinetics: Unfractionated Heparin

A

Short T1/2 of approx 2 hours. The drug can be given SC or IV bolus and infusion.

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8
Q

The drug requires frequent monitoring with activated partial thromboplastin time (aPTT). The levels of aPTT need to be evaluated ever 6 hours to ensure the drug falls into the range of 1.5 to 2.5 times the control (per lab)

A

Unfractionated Heparin

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9
Q

Unfractionated Heparin can be reversed by

A

Protamine

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10
Q

MOA: Enoxaparin (IV only)

A

Inhibition of factor Xa (and thrombin)

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11
Q

IV only drugs with a longer T1/2. Less bound to plasma proteins and endothelial cells giving them more predictable dosing and activity. Eliminated via the kidneys, therefore will require adjustment in renal disease and contraindicated in hemodialysis (HD) patients

A

Enoxaparin, Dalteparin, and Tinzaparin

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12
Q

MOA: Dalteparin (IV only)

A

Inhibition of factor Xa (and thrombin)

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13
Q

No required monitoring involved, however can be monitored by evaluating anti-Xa levels to assess activity

A

Enoxaparin, Dalteparin, and Tinzaparin

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14
Q

MOA: Tinzaparin (IV only)

A

Inhibition of factor Xa (and thrombin)

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15
Q

Uses: DVT prophylaxis, DVT or PE treatment, AMI, and used during PCI in the coronary cath-lab

A

Enoxaparin, Dalteparin, and Tinzaparin

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16
Q

Uses: AMI, DVT prophylaxis, DVT or PE, and stroke. Also may be used to transition patients as they await the INR to raise from warfarin therapy. Useful for anticoagulation during open-heart surgery

A

Unfractionated Heparin

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17
Q

Adverse events: Enoxaparin, Dalteparin, and Tinzaparin

A

Bleeding, lower incidence of causing thrombocytopenia than heparin

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18
Q

Adverse events: Unfractionated Heparin

A

Bleeding, thrombocytopenia, hypersensistivity reaction, and long-term use is associated with osteoporosis (secondary to activity on osteoclasts/osteoblasts)

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19
Q

Synthetically manufactured, intravenous infusion given to patients requiring anticoagulation therapy. Infusion therapy is titrated to aPPT, similar to heparin.

A

Argatroban

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20
Q

Dosing adjustment: Argatroban (IV only)

A

Required for hepatic dysfunction

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21
Q

Leech-saliva derived, intravenous infusion given to patients requiring anticoagulation. Infusion is titrated to aPPT, similar to UFH.

A

Lepirudin

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22
Q

Dosing adjustment: Lepirudin (IV only)

A

Required for patients with renal dysfunction

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23
Q

Synthetically manufactured, intravenous infusion. Can be utilized for patients requiring acute coronary syndrome treatment via Percutaneous coronary intervention. The infusion is given as a bolus and infusion dosing.

A

Bivalrudin

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24
Q

IV only Direct Thrombin Inhibitors

A

Argatroban, Lepirudin, and Bivalrudin

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25
Q

MOA: Warfarin

A

Inhibition of hepatic-vitamin K dependent clotting factors (II, VII, IX, and X). The reduced form of vitamin K is required for gamma-carboxylation of these clotting factors. Warfarin inhibits vitamin K reductase, inhibiting the conversion of vitamin K to the reduced form, and thus inhibiting the production of II, VII, IX, and X

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26
Q

Warfarin has 2 isomers. What are they and which one is more potent

A

(R-) and (S-) isomers. The (S-) isomer is more potent.

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27
Q

Kinetics: Warfarin

A

Long-acting therapy. Drug is primarily protein bound (greater than 90%).

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28
Q

Metabolism: Warfarin

A

Warfarin has 2 isomers (R-) and (S-) formations. The (S-) isomer is more potent. Metabolism of the (S-) is via CYP 2C9 and (R-) is CYP 3A4

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29
Q

Drug can also cross the placenta, therefore contraindicated in pregnancy

A

Warfarin

30
Q

Indications: Long-term outpatient anticoagulation with oral therapy for treatment of DVT, PE, stroke, anticoagulation required for patients with atrial fibrillation, and for inherited clotting disorders (Protein C and S deficiencies)

A

Warfarin

31
Q

Prothrombin time (PT) is not standardized lab value. What is a lab standard that patients can have measured in any laboratory

A

International normalized ratio (INR). Monitoring range is dependent on the disease state (ie DVT or PE range of 2-3, but for mechanical heart valve range goal (2.5 to 3.5)

32
Q

Oral direct thrombin inhibitor pro-drug with lower potential to need extensive monitoring and drug interactions.

A

Dabigatran

33
Q

Dabigatran is reversed by

A

There is no specific way exists to reverse the anticoagulant effect of dabigatran in the event of a major bleeding event

34
Q

MOA: Apixaban

A

Oral direct Xa inhibitors (act directly for the inhibition of factor Xa)

35
Q

MOA: Rivaroxaban

A

Oral direct Xa inhibitors (act directly for the inhibition of factor Xa)

36
Q

Can cause an antigenic activity as it is derived from B-hemolytic streptococci

A

Streptokinase

37
Q

MOA: Streptokinase

A

It binds to Plasminogen to form a complex that converts substrate plasminogen to plasmin

38
Q

This is a recombinant tissue plasminogen activator. FDA-approved for treatment of myocardial infarction with ST-elevation, but also many other indications where thrombolytic therapy is needed

A

Alteplase

39
Q

MOA: Alteplase

A

Tissue plasminogen activator is a protein involved in the breakdown of blood clots. It is a serine protease found on endothelial cells. It catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

40
Q

This is a recombinant tissue plasminogen activator. FDA-approved for acute myocardial infarction, where it shows fewer bleeding complications but otherwise similar mortality rates after one year compared to alteplase

A

Tenecteplase

41
Q

MOA: Tenecteplase

A

Tissue plasminogen activator is a protein involved in the breakdown of blood clots. It is a serine protease found on endothelial cells. It catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

42
Q

This is a recombinant tissue plasminogen activator. FDA-approved for acute myocardial infarction, where it has more convenient administration and faster thrombolysis than Alteplase

A

Reteplase

43
Q

MOA: Reteplase

A

Tissue plasminogen activator is a protein involved in the breakdown of blood clots. It is a serine protease found on endothelial cells. It catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown.

44
Q

Irreversible inhibition of COX in platelets which will lead to decreased activation

A

ASA

45
Q

Used for prophylaxis for AMI and/or the first dose for the event.

A

ASA

46
Q

MOA: Ticlopidine

A

ADP inhibitors- blockade of the P2Y12 receptors on platelets to decrease their activation by ADP. This prevents ADP-induced activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen and to each other

47
Q

What order is consistent with their onset of action from slowest to fastest on inhibition of platelet activation when the loading doses are used

A

Ticlopidine (Slowest), clopidogrel, and prasugrel (Fastest)

48
Q

The notable adverse reaction of ticlopidine is

A

Thrombocytopenic purpura (TTP)

49
Q

MOA: Clopidogrel

A

ADP inhibitors- blockade of the P2Y12 receptors on platelets to decrease their activation by ADP. This prevents ADP-induced activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen and to each other

50
Q

Why do ADP inhibitors have drug interaction with proton pump inhibitors

A

Since the PPI’s are metabolized and serve as substrates via 2C19; therefore there is science that there is competitive inhibition which could potentially result in lower concentrations of ADP antagonists, particularly ticlopidine and clopidogrel.

51
Q

MOA: Prasugrel

A

ADP inhibitors- blockade of the P2Y12 receptors on platelets to decrease their activation by ADP. This prevents ADP-induced activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen and to each other

52
Q

MOA: Abciximab

A

Glycoprotein (GP) IIb/IIIa receptor inhibitor (> 80% blockade results in activity). They work by preventing platelet aggregation and thrombus formation by inhibition of the GpIIb/IIIa receptor on the surface of the platelets. The GP IIb/IIIa receptors are the final step in platelet-platelet aggregation.

53
Q

Uses: Abciximab, Eptifibatide, and Tirofiban

A

These drugs are used for medical management of acute coronary syndrome (ACS) and are indicated for cases during the PCI-Cath lab procedures

54
Q

Indicated for cases during the PCI-Cath lab procedures. Drug involves hepatic metabolism and given as intravenous bolus and infusion. In addition, the drug’s metabolism occurs via the reticular endothelial system (RES) and dosing adjustment not needed for renal dysfunction.

A

Abciximab

55
Q

MOA: Eptifibatide

A

Glycoprotein (GP) IIb/IIIa receptor inhibitor (> 80% blockade results in activity). They work by preventing platelet aggregation and thrombus formation by inhibition of the GpIIb/IIIa receptor on the surface of the platelets. The GP IIb/IIIa receptors are the final step in platelet-platelet aggregation.

56
Q

MOA: Tirofiban

A

Glycoprotein (GP) IIb/IIIa receptor inhibitor (> 80% blockade results in activity). They work by preventing platelet aggregation and thrombus formation by inhibition of the GpIIb/IIIa receptor on the surface of the platelets. The GP IIb/IIIa receptors are the final step in platelet-platelet aggregation.

57
Q

Indicated for cases during the PCI-Cath lab and for medical management. Given as an intravenous bolus and infusion and does require dosing adjustment for renal dysfunction

A

Tirofiban and Eptifibatide

58
Q

When does warfarin begin to have an effect

A

3-5 days after administration

59
Q

What reverses the effects of warfarin

A

Vitamin K

60
Q

What are the half lives of factors VII, IX, X, and II

A

VII: 6-7 hours, IX: 24 hours, X: 40 hours, II: 60 hours

61
Q

What natural anticoagulant factor is also vitamin K dependent and inhibited by warfarin.

A

Protein C. It has a short half life like factor VII so early in warfarin therapy, patients may experience a paradoxical hypercoagulable state.

62
Q

Name the oral Xa inhibitor(s)

A

Rivaroxaban and Apixaban

63
Q

Name the intravenous Xa inhibitor(s)

A

Enoxaparin, Dalteparin, and Tinzaparin

64
Q

Name the oral thrombin inhibitor(s)

A

Dabigatran

65
Q

Name the intravenous thrombin inhibitor(s)

A

Argatroban, Lepirudin, and Bivalrudin

66
Q

What reverses the action of alteplase, tenecteplase, and reteplase

A

Cryoprecipitate (lots of fibrinogen), Aminocaproic acid, or Tranexamic acid

67
Q

What is given in place of aspirin to a patient with an aspirin allergy

A

Clopidogrel or Prasugrel. Ticlopidine is used far less frequently

68
Q

MOA: Dipyridamole

A

Coronary vasodilation by inhibiting the cellular uptake of adenosine. It also has some weak antiplatelet activity by increasing intracellular cAMP through the inhibition of the phosphodiesterase enzyme, resulting in decreased Thromboxane A2 synthesis

69
Q

What is usually given in combination with Aspirin because it is ineffective alone

A

Dipyridamole

70
Q

Which GP IIb/IIIa inhibitors are long vs short acting

A

long acting (18-24 hrs): Abciximab. Short acting (6-12 hrs): Tirofiban and Eptifibatide

71
Q

What is Abciximab usually administered with

A

Heparin or aspirin

Heme (7 decks)

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