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Pharmacology > EXAM #2: HEMATOLOGICAL AGENTS II > Flashcards

EXAM #2: HEMATOLOGICAL AGENTS II Flashcards

1
Q

What is Type I HIT?

A

Heparin Induced Thrombocytopenia
- Decreased platelet numbers in first 2-5 days of treatment

Not of much clinical consequence*

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2
Q

What is Type II HIT?

A

Uncommon but SERIOUS Heparin Induced Thrombocytopenia

  • Heparin binds platelet factor 4 (PF4)
  • Antibodies formed against PF4/Heparin
  • Antibodies activates platelets can cause their consumption by splenic macrophages

Result is BOTH thrombocytopenia and thrombosis*

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3
Q

What type of heparin causes HIT Type II?

A

Unfractionated/ HMW

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4
Q

What patient populations is Type II HIT seen in most often?

A

1) Surgical
2) Cancer
3) Women

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5
Q

What is Enoxaparain?

A

LMW Heparin (Lovenox)

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6
Q

What are the advantages of LMWH vs. HMWH?

A

1) Easier to dose
2) Less risk of HIT
3) Less risk of osteoporosis

LMWH is generally safer than HMWH

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7
Q

What is the contraindication for LMWH?

A

LMWH is cleared by the kidneys; thus, NOT indicated in patients with severe renal insufficiency

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8
Q

What is the disadvantage of LMWH?

A

Protamine only PARTIALLY reverses it

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9
Q

What is the mechanism of action of Fondaparinux?

A

Synthetic analog of the antithrombin binding pentasaccharide sequence of Heparin

Cannot bridge AT and Thrombin like Heparin

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10
Q

Can Protamine be used to reverse Fondaparinux?

A

NO

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11
Q

In what patients is Fondaparinux contraindicated?

A

Severe renal insufficiency

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12
Q

What assay is used to monitor LMWH and Fondaparinux?

A

Anti-factor Xa Assay

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13
Q

List the direct thrombin inhibitors (DTIs).

A

Argatroban
Bivalrudin
Dabigatron
Lepirudin

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14
Q

What is the mechanism of action of the direct thrombin inhibitors?

A
  • Bind either fibrin binding (active site) of thrombin or,

- Bind BOTH E1 and active site, fibrin binding site of thrombin

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15
Q

What are the univalent DTIs?

A

These are the direct thrombin inhibitors that only bind at the active site, i.e. the fibrinogen binding site

  • Aragatroban
  • Dabigatran

“an”= univalent

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16
Q

What are the divalent DTIs?

A

These are the direct thrombin inhibitors that only bind at BOTH the active site and E1

  • Bivalrudin
  • Lepirudin

“din”= DIvalent/ bivalent

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17
Q

List the DTIs that can be given parenterally.

A

Aragatroban
Bivalrudin
Lepirudin

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18
Q

What DTI can be given orally?

A

Dabigatran

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19
Q

What is the major advantage of DTIs over Heparin?

A
  • Heparin CANNOT inhibit thrombin bound to fibrin

- DTIs CAN inhibit thrombin bound to heparin

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20
Q

What DTIs are used to treat HIT?

A

All BUT Dabigatran

  • Bivalrudin
  • Lepirudin
  • Aragatroban
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21
Q

What DTI is used to treat CVA?

A

Dabigatran

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22
Q

What DTI is used for PCI and HIT in patients undergoing PCI?

A

Bivalirudin

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23
Q

What is the drawback to the DTIs?

A

No antidote as there is with Heparin

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24
Q

What are the indications for Warfarin?

A

Venous thrombosis or thromboembolism

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25
Q

What is the mechanism of action of Warfarin?

A

Competes with Vitamin K for Vitamin K reductase

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26
Q

What is the normal role of Vitamin K in clotting?

A

Activation of II, VII, IX, X and Protein C and S are Vitamin K dependent

27
Q

How long does it take for Warfarin to start working? Why?

A

3-5 days b/c Warfarin cannot reduce the activity of PREVIOUSLY SYNTHESIZED coagulation factors

28
Q

How is the 3-5 day onset of action of Warfarin combated in the clinical setting?

A

Bridge with LMWH (Lovenox)

29
Q

What enzyme metabolizes Warfarin? Why is this important?

A

CYP2C9

  • High genetic polymorphisms that can alter dosing in patients
30
Q

What assay is used to monitor Warfarin?

A

PT/INR

Prothrombin time*

31
Q

What is the normal/target INR with Warfarin therapy?

A

2.0-3.0

32
Q

What is the effect of broad spectrum antibiotics on Warfarin therapy?

A

Increases the effect of Warfarin by decreasing endogenous Vitamin K

33
Q

What is the effect of NSAIDs on Warfarin therapy?

A

Interfere with primary hemostasis and increase effects

34
Q

What is the effect of SSRIs on Warfarin therapy?

A

Interfere with primary hemostasis and increase effects

35
Q

What is the effect of certain statins on Warfarin therapy?

A

Decrease hepatic metabolism and increase effects

36
Q

What is the effect of Rifampin on Warfarin therapy?

A

Increases hepatic metabolism and decreases effects

37
Q

What is the effect of barbiturates on Warfarin therapy?

A

Increases hepatic metabolism and decreases effects

38
Q

What is the effect of Carbamazepine on Warfarin therapy?

A

Increases hepatic metabolism and decreases effects

39
Q

What is the effect of drugs that potentiate warfarin’s effects on PT/INR?

A

Increase INR

40
Q

What is the effect of drugs that inhibit warfarin’s effects on PT/INR?

A

Decrease INR

41
Q

What is the effect of impaired hepatic function of warfarin?

A
  • Decreased clearance

- Increased INR

42
Q

What is the effect of Crohn’s Disease that reduce Vitamin K on warfarin therapy?

A

Increase INR

43
Q

What are the clinical considerations in patients with renal insufficiency and Warfarin?

A
  • Renal insufficiency can cause hypoalbuminemia

- This will INCREASE the INR

44
Q

What are the adverse effects of Warfarin?

A

1) Hemorrhage
2) Placental transfer
3) Birth defects
4) Warfarin necrosis (caused by a drop in Protein C)

45
Q

How can the effects of Warfarin therapy be reversed?

A

1) Vitamin K

2) Plasma transfusion

46
Q

What are the limitations and challenges associated with Warfarin?

A

1) Narrow TI
2) Long half-life
3) Slow onset of action

47
Q

List the new oral anticoagulants.

A

1) Rivaroxaban
2) Apixaban
3) Dabigatran

48
Q

What are the benefits of the new oral anticoagulants compared to Warfarin?

A

1) Faster onset
2) Larger TI
3) Low potential for food and drug interactions
4) Predicatable anticoagulant effects that limits need for blood monitoring
5) Less overall bleeding risk

49
Q

What is the mechanism of action for Rivaroxaban?

A

Oral direct Xa inhibitor

50
Q

What should be remembered about Riavorxaban in the treatment of PE?

A

As efficacious in the treatment of PE as warfarin/heparin bridge, but LESS major bleeding

51
Q

What is the mechanism of action of Dabigatran?

A

Oral thrombin inhibitor

52
Q

What is the contraindication of Dabigatran?

A

Mechanical heart valve

53
Q

Which class of anticogulants is safe to use druing pregnancy?

A

Heparin

Rivaroxaban and apixaban are “use with caution”

54
Q

What is the main enzyme that breaks down the fibrin clot? What is its precuror?

A

Plasminogen–>plasmin

  • Plasmin is the enzyme that breaks down the fibrin clot
55
Q

What factors activate plasminogen to plasmin?

A

tPA

u-PA

56
Q

What is unique about the selectivity of tPA?

A

tPA has a high affinity for fibrin, which prevents plasminogen from being activated randomly in the bloodstream

57
Q

List the fibrinolytic drugs.

A

1) Streptokinase
2) u-PA
3) t-PA
- Endogenous
- Alteplase
- Reteplase
- Tenecteplase

58
Q

What is the mechanism of action of Streptokinase?

A
  • Forms a complex with plasminogen

- Streptokinase/plasminogen activate free plasminogen to plasmin

59
Q

What is the drawback associated with Streptokinase?

A
  • Tolerance

- Hypersensitivity with repeated use

60
Q

What are the indications for tPA e.g. altepalse?

A

STEMI within 12 hour onset

CVA

61
Q

What are the absolute contraindications to thrombolytic therapy?

A

1) Greater than 24 hours from onset
2) Prior intracranial hemorrhage
3) CVA within last year
4) Intracranial neoplasm
5) Active bleeding
6) Aortic dissection
7) Head or facial trauma within the past 3 months

62
Q

List the inhibitors of fibrinolysis.

A

Aminocaproic acid

Tranexamic acid

63
Q

What are inhibitors of fibrinolysis used to treat?

A

1) Hemophilia

2) Reverse bleeding from fibrinolytic therapy

64
Q

What is the mechanism of action of the inhibitors of fibrinolysis?

A

Block the interaction of plasmin with fibrin i.e. plasmin cannot degrade the fibrin clot

Pharmacology (64 decks)

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