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PNS/Cardiology > Anticoagulant Drugs > Flashcards

Anticoagulant Drugs Flashcards

1
Q

What are the Factor Xa inhibitors?

A

Unfractioned heparin
Low molecular weight heparin (Enoxaparin)
Rivaroxaban
Apixaban

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2
Q

What are vitamin K antagonist anticoagulants?

A

Warfarin

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3
Q

What are direct thrombin inhibitors?

A

Bivalirudin

Dabigatran

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4
Q

What is the mechanism of unfractionated heparin?

A

Binds antithrombin (AT), producing conformational change that makes AT reactive site more accessible and able to inactivate thrombin (Factor II) and Factor Xa

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5
Q

What determines if a heparin molecule will inactivate thrombin (Factor II) or Factor Xa?

A

Heparin binds to anti-thrombin with unique pentasaccharide sequence
Binding to thrombin requires minimum of 13 additional saccharide units
If less than 13 additional units, will bind Factor Xa

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6
Q

What mechanism clears low doses of heparin?

A

Rapid, saturable (cellular) mechanism of clearance

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7
Q

What mechanism clears high doses of heparin?

A

Slow, nonsaturable renal mechanism of clearance

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8
Q

What mechanism clears therapeutic doses of heparin?

A

Combination of rapid, saturable mechanism and slower, nonsaturable renal mechanism

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9
Q

Does the half life of heparin increase or decrease in patients with pulmonary embolism?

A

Decrease (need to give more heparin)

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10
Q

Does the half life of heparin increase or decrease in patients with advanced renal disease?

A

Increase (need to give less heparin)

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11
Q

Why can heparin be a difficult/lousy drug?

A

Variability in anticoagulant response due to variable binding to plasma proteins
Requires close monitoring of aPTT

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12
Q

What are routes of administration of heparin?

A

Continuous infusion

Subcutaneous administration

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13
Q

What are major complications of unfractioned heparin?

A

BLEEDING

Thrombocytopenia

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14
Q

How does low molecular weight heparin (LMWH) differ from unfractioned heparin?

A

Shorter than unfractioned heparin, so most do not contain the 13 saccharide units necessary to bind thrombin
Hence, has greater activity against Factor Xa (does not require 13 saccharide units)

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15
Q

Why does LMWH have a more predictable anticoagulant response than unfractioned heparin?

A

LMWH binds to less plasma proteins and proteins released from activated platelets and endothelial cells
Do not need PTT for it

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16
Q

What are complications of LMWH?

A

Bleeding

Less thrombocytopenia than unfractioned heparin

17
Q

What is the most common LMWH used clinically?

A

Enoxaparin (Lovenox)

18
Q

Why is unfractioned heparin still used for acute coronary syndrome if LMWH may be better?

A

Allows monitoring of aPTTs throughout treatment

Can tell if treatment is working

19
Q

What are clinical uses of heparin?

A

Acute coronary syndrome
Venous thromboembolitic disease (DVT or PE)
Cerebrovascular disease

20
Q

What is the mechanism of action of Rivaroxaban and Apixaban?

A

Oral Factor Xa inhibitors that selectively block active site of Factor Xa
Do not require a cofactor (like antithrombin) for activity

21
Q

What are clinical uses of Rivaroxaban and Apixaban?

A

Reduction of stroke and embolism in non-valvular A-fib
Prophylaxis of DVT in knee/hip surgery
Treatment of DVT and PE and prevention of recurrence

22
Q

When should Rivaroxaban be taken?

A

With evening meal (bioavailability enhanced with food)

23
Q

What is the mechanism of action of Warfarin?

A

Binds and inhibits vitamin K epoxide reductase (VKOR)
VKOR regenerates reduced vitamin K
Vitamin K is cofactor for synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X) and anti-coagulant proteins C and S

Inhibited VKOR –> reduced NEW clotting factors

24
Q

What is the anticoagulant effect of warfarin dependent on?

A

The clearance of functional clotting factors (II, VII, IX, X)

Warfarin will only exert effect on production of new clotting factors, so will only see anticoagulation once existing functional clotting factors are cleared (4-5 days)

25
Q

What are clinical indications for warfarin?

A

Treatment and prevention of DVT/PE
Prosthetic heart valves
Stroke prevention in A-fib/flutter

26
Q

What are complications of warfarin?

A

Bleeding (if major bleeding can reverse with vitamin K of infusion of clotting factors with fresh frozen plasma)
Skin necrosis
Drug-drug interactions

27
Q

What is the mechanism of action of Dabigatran?

A

Competitive, direct thrombin (Factor II) inhibitor

Inhibits both free and clot-bound thrombin (non-specific)

28
Q

Is dabigatran IV or PO?

A

PO

29
Q

What is the mechanism of action of Bivalirudin?

A

Block active site of thrombin
and/or
Prevent substrates from binding to the substrate recognition site

No additional cofactors needed
Inhibits both free and clot-bound thrombin (non-specific)

30
Q

When is bivalirudin used?

A

Patients undergoing PCI

Heparin also used in this situation but bivalirudin can have reduced level of bleeding so might be better

31
Q

What is a major difference between heparin/warfarin and fibrinolytics?

A

Heparin/warfarin do not dissolve clots!! Prevents clot from getting bigger and allows body to reabsorb it

Fibrinolytics dissolve the clots

32
Q

What is the mechanism of streptokinase?

A

Complexes with plasminogen and activates plasmin

Plasmin –> digests circulating fibrinogen

33
Q

What is an adverse effect of streptokinase?

A

Allergic reactions since previous exposure to streptokinase when get strep infection

34
Q

What is the mechanism of tissue plasminogen activator (TPA)?

A

Binds fibrin, activating bound plasminogen

Activates bound plasminogen much more rapidly than plasminogen in circulation (absence of fibrin)

Hence is clot specific

35
Q

How does recombinant plasminogen activator (r-PA) and TNK-t-PA differ from Tissue Plasminogen activator?

A

Structure change gives a longer half-life

Longer half-life facilitate bolus administration primarily for STEMI

36
Q

What are clinical uses of fibrinolytic drugs?

A

Venous thromboembolism (DVT, mostly PE)
STEMI
Stroke

37
Q

What are major contraindications to fibrinolytic therapy?

A

Surgery within 10 days
Serious gastrointestinal bleeding within 3 months
History of hypertension (diastolic pressure > 110 mm Hg)
Active bleeding or hemorrhagic disorder
Previous cerebrovascular accident or active intracranial process
Aortic dissection
Acute pericarditis

PNS/Cardiology (33 decks)

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