Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drug Mechanisms > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

What are the different classes of anticoagulants?

A
  1. Indirect thrombin inhibitors
  2. Direct thrombin inhibitors
  3. Indirect factor Xa inhibitors
  4. Direct factor Xa inhibitors
  5. Fibrinolytic agents
  6. Vitamin K antagonists
  7. Antiplatelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two indirect thrombin inhibitors?

A

Unfractionated heparin and low molecular weight heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

They bind to antithrombin causing a conformational change. This conformation change allows antithrombin to rapidly bind to factors IIa and Xa and inhibit their function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the activity for UFH?

A

It has a high affinity for antithrombin and can inhibit both factor IIa and Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the activity for LMWH?

A

It is made up of fragments of UFH; therefore, it has a lower affinity for antithrombin and can inhibit factor Xa but has little inhibitory effect on IIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the toxicities associated with indirect thrombin inhibitors?

A
  1. Bleeding
  2. Thrombocytopenia
  3. Caution w/ allergies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is heparin made up of?

A

Sulfated mucopolysaccharides that are very acidic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is heparin used to treat?

A

Full dose IV: venous thrombosis and pulmonary embolism

Lower dose SC: after surgery in high risk patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the antidote for heparin?

A

Protamine sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does protamine sulfate work?

A

It binds to heparin forming an inactivated salt that is excreted by the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the advantages of LMWH?

A
  1. Greater bioavailability with SC; therefore, it has a more predictive anticoagulant response
  2. Longer half-life and less frequent dosing
  3. Three available preparations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the advantages of UFH?

A
  1. Rapid reversal of anticoagulant effect with protamine sulfate
  2. Doesn’t get clear by kidneys and may be safer in patients with renal insufficiencies
  3. Direct inhibitor of the contact activation pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the disadvantages of UFH?

A
  1. More likely to cause heparin induced thrombocytopenia

2. More variable anticoagulant response that requires monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drug is a direct thrombin inhibitor?

A

Dabigatran (Pradaxa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the activity of Dabigitran?

A

It is used to prevent thromboembolic disorders such as venous thromboembolism, DVT, and thromboemobolic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What types of thrombin does dabigatran inhibit?

A

fibrin bound and free thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mechanism of action of Dabigatran?

A

It is a potent, competitive, reversible inhibitor that binds to the active site of thrombin and inhibits its effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the toxicities associated with Dabigatran?

A
  1. Dyspepsia
  2. Gastritis
  3. Bleeding (higher risk of general and GI bleeding than warfarin)
  4. Hemorrhagic stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Does Dabigatran require monitoring?

A

No, it’s effects are less variable than warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Does dabigatran require a modified diet?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the half-life of dabigatran compared to warfarin?

A

It has a shorter half-life; therefore, missed doses could increase risk of thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the antidote for dabigatran?

A

Idarucizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Can dabigatran’s anticoagulant properties be measured during therapy?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What drug is an indirect factor Xa inhibitor?

A

Fondaparinux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the activity of fondaparinux?

A

It’s as safe and effective as UFH and LMWH in the prophylaxis and treatment of venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the mechanism of action of fondaparinux?

A

It binds to antithrombin and indirectly inhibits factor Xa. This inhibits thrombin production in both pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the toxicities associated with fondaparinux?

A

Much less likely to cause heparin-induced thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is fondaparinux (structural level)?

A

A synthetic analog of the pentasaccharide sequence of heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What type of factor can fondaparinux, UFH, and LMWH inhibit?

A

Only free circulating factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What drug is a direct factor Xa inhibitor?

A

Rivaroxaban

31
Q

What is the activity of Rivaroxaban?

A

Used in the treatment of venous thromboembolism including DVT and pulmonary embolism. Also used in preventing strokes in patients with atrial fibrillation.

32
Q

What is the mechanism of action for Rivaroxaban?

A

Highly selective, competitive, reversible inhibitor of free circulating and fibrin-bound factor Xa which inhibits the production of thrombin in both pathways

33
Q

What are the toxicities associated with Rivaroxaban?

A
  1. Bleeding

2. Monitoring of renal function

34
Q

Does Rivaroxaban require dietary modifications?

A

No

35
Q

How does the half-life of Rivaroxaban compare to warfarin?

A

It has a shorter half-life; therefore, missed doses increase the risk of thrombosis

36
Q

Can Rivaroxaban’s anticoagulant properties be measured during therapy?

A

No

37
Q

What is the antidote for Rivaroxaban?

A

Andexanet Alfa

38
Q

What does Andexanet Alfa do?

A

It is a factor Xa decoy that neutralizes direct factor Xa inhibitors

39
Q

What are the fibrinolytic agents?

A
  1. Streptokinase
  2. Urokinase
  3. Tissue Plasminogen Activator (“teplase” ending)
40
Q

What are the indications for the fibrinolytic agents?

A

Used for the treatment of thrombotic diseases and management of acute myocardial infarction

41
Q

What is the mechanism of action of streptokinase?

A

Binds to pro-activator plasminogen to form a complex that catalyzes the conversion of inactive plasminogen to active plasmin.

42
Q

What is the mechanism of action of Urokinase?

A

Directly converts plasminogen to active plasmin

43
Q

What is the mechanism of action of Tissue Plasminogen Activator?

A

Preferentially activates plasminogen that is bound to fibrin

44
Q

Where is urokinase synthesized?

A

The kidney

45
Q

What is the difference between Alteplase, Reteplase, and Tenecteplase?

A

Alteplase: recombinant human t-PA
Reteplase: recombinant human t-PA that is less fibrin specific
Tenecteplase: mutant form of t-PA that has longer half-life and is slightly more fibrin-specific than t-PA

46
Q

What drug is a Vitamin K antagonist?

A

Warfarin

47
Q

What are the indications for warfarin?

A

It can be used along or in combination with heparin for prophylaxis and treatment of intravascular clotting

48
Q

Which enantiomer of warfarin is stronger?

A

The S enantiomer is 3-5 times more potent

49
Q

What is the mechanism of action of warfarin?

A

It inhibits the vitamin K epoxide reductase enzyme which prevents vitamin K from being produce. This blocks the carboxylation of clotting factors II, VII, IX, and X forming inactive molecules

50
Q

How long is the delay in warfarin’s anticoagulant effect?

A

8-12 due to the time it takes to degrade clotting factors

51
Q

Can warfarin effect an already formed embolism?

A

No, but it can prevent further clotting

52
Q

What are the toxicities associated with warfarin?

A
  1. Bleeding

2. Can cross placenta causing hemorrhagic disorder

53
Q

What are the 8 interactions that can alter the effects of warfarin?

A
  1. Aspirin
  2. Heparin
  3. 3rd generation cephalosporins
  4. Hepatic disease
  5. Hyperthyroidism
  6. Hypothyroidism
  7. Diuretics
  8. Vitamin K
54
Q

What effect does aspirin have on warfarin?

A

increases anticoagulant effects by affecting platelet function

55
Q

What effect does heparin have on warfarin?

A

increases anticoagulant effect by inhibiting several clotting factors

56
Q

What effect do 3rd generation cephalosporins have on warfarin?

A

increase anticoagulant effect by eliminating bacterial microflora that produce vitamin K

57
Q

What effect does hyperthyroidism have on warfarin?

A

increase anticoagulant effect by increasing the degradation of clotting factors

58
Q

What effect does hypothyroidism have on warfarin?

A

decreases anticoagulant effect by decreasing the turnover rate of clotting factors

59
Q

What effect does hepatic disease have on warfarin?

A

increases anticoagulant effect by inhibiting the synthesis of clotting factors in the liver

60
Q

What effect does vitamin K have on warfarin?

A

decreases anticoagulant effect by increasing the production of clotting factors

61
Q

What effect do diuretics have on warfarin?

A

decrease anticoagulant effect by increasing the concentration of clotting factors in circulation

62
Q

What do genes have the most effect on warfarin response?

A

CYP2C9 and VKORC1

63
Q

Variants of which gene are more prevalent?

A

VKORC1

64
Q

Which gene has a greater effect on warfarin?

A

VKORC1

65
Q

What should you do with the warfarin dose when dealing with variations in the CYP2C9 and VKORC1 genes?

A

Decrease the dose

66
Q

What is the antidote for warfarin?

A

Phytonadione, fresh-frozen plasma, prothrombin complex concentrates, and recombinant clotting factor VIIa

67
Q

How long does it take the antidote to fully restore vitamin K-dependent clotting factors?

A

24 hours

68
Q

What is the negative aspect to FFP?

A

It requires blood group typing, thawing, and large volumes of fluid which can overload elderly patients and those with heart disease

69
Q

What is included in 3-factor PCC?

A

Factors II, IX, and X

70
Q

What is included in 4-factor PCC?

A

Factors II, VII, IX, and X

71
Q

What can occur with the use of antidotes?

A

Fatal venous and arterial thromboembolic complications

72
Q

What are the anti-platelet agents?

A
  1. Aspirin
  2. Thienopyridines
  3. Cyclopentyltriaxolopyrimidines
  4. Nonthienopyridine ATP analogs
  5. GP IIb/IIIa receptor antagonists
  6. PAR-1 antagonists
  7. Dipyridamole
73
Q

What is the activity of aspirin?

A
  1. Prophylaxis

Drug Mechanisms (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions