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Essential Hematology > Chapter 25: Thrombosis and antithrombotic therapy > Flashcards

Chapter 25: Thrombosis and antithrombotic therapy Flashcards

1
Q

What is thrombophilia?

A

Thrombophilia are inherited or acquired disorders that predispose to thrombosis?

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2
Q

What are the strongest independent predictors of coronary events?

A

The levels of factor VII and fibrinogen. Hyperhomocysteinemia has also been associated with increased risk.

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3
Q

What is Virchow’s triad?

A

Virchow’s triad is composed of three components that are extremely important for thrombus formation.

(1) Slowing of blood flow
(2) hypercoagulability of the blood
(3) Vessel wall damage.

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4
Q

What events suggest a hereditary thrombophilia?

A

Younger patients that suffer from spontaneous and recurrent thromboses in abnormal locations.

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5
Q

What is the most common disorder that increases the risk of thrombosis?

A

Factor V leiden mutation. (4% of caucasians)

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6
Q

With what protein deficiency is skin necrosis due to dermal vessel occlusion after warfarin administration associated?

A

Protein C deficiency

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7
Q

Why does warfarin cause vessel occlusion associated with protein C deficiency?

A

Because Warfarin inhibits vitamin K dependent factors. Vitamin K is necessary for protein C to function.

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8
Q

How does prothrombin allele G20210A lead to thrombophilia?

A

There is increased levels of prothrombin which leads to increased thrombin and down regulation of fibrinolysis.

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9
Q

What enzyme is responsible for hyperhomocysteinemia?

A

A defect in cystathione beta synthase is responsible for hyperhomocysteinemia.

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10
Q

What are some causes of acquired hyperhomocysteinemia?

A

(1) Folate or B12 deficiency
(2) B6 deficiency
(3) drugs (ciclosporin)
(4) renal damage.
(5) smoking.

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11
Q

Do defects in fibrinogen lead to thrombosis?

A

Not usually, bleeding is more likely.

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12
Q

What are some common acquired risk factors for thrombosis?

A

(1) surgical opperations
(2) Venous stasis and immobility
(3) Malignancy
(4) Inflammation
(5) polycythemia and ET
(6) increased estrogen

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13
Q

What is antiphospholipid syndrome?

A

The occurrence of repeated thromboses/miscarriages with the presence of anti phospholipid antibodies. These antibodies are in some cases secondary to autoimmune disease.

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14
Q

Why does glucosylceremide deficiency lead to thrombosis?

A

Because glucosylceremide modulates the protein C pathway.

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15
Q

Why are factor IX concentrates sometimes complicated by thrombosis?

A

Because factor IX concentrates often contain activated coagulation factors.

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16
Q

What factors should increase the clinical suspicion of deep vein thrombosis?

A

Bedridden patients with unilateral swelling or tenderness.

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17
Q

What is the first line test when DVT is suspected?

A

Serial compression ultrasonography

18
Q

What is the second line test if ultrasonography is negative yet clinical signs point to DVT?

A

Contrast venography

19
Q

What is a plasma D-dimer concentration assay?

A

Plasma D-dimers are the breakdown products of fresh thromboses. They are elevated if DVT has occured. However they may be elevated in some other conditions as well.

20
Q

When should a pulmonary embolus be suspected?

A

When the patient has

(1) history of DVT
(2) immobilization for more than 2 Days
(3) surgery
(4) hemoptysis

21
Q

What methods may be used to diagnose pulmonary embolism?

A

(1) chest X-ray
(2) ventilation perfusion scintigraphy
(3) Computed tomography pulmonary angiographty
(4) MRI angiography
(5) Pulmonary angiography

22
Q

How is heparin administered?

A

intravenously

23
Q

How is heparin eliminated by the body?

A

Heparin is inactivated by the liver and excreted in the urine.

24
Q

What is the biological half-life of heparin?

A

Approximately 1 hour.

25
Q

What is heparin’s mechanism of action?

A

Heparin potentiates the formation of complexes between antithrombin and thrombin, IXa, Xa, and XIa. This leads to the irreversible inactivation of these factors.

26
Q

What are the indications for Heparin?

A

(1) DVT
(2) Pulmonary embolism
(3) unstable angina pectoris
(4) Prophylaxis during pregnancy (does not cross the placenta)

27
Q

What is the treatment of choice for acute pulmonary embolus?

A

Continuous intravenous heparin

28
Q

What is the preferred prophylacitic treatment for venous thrombosis?

A

Intermittent subcutaneous heparin.

29
Q

What is the difference between regular heparin and low molecular weight fractionated heparin?

A

LMWFH has a longer half life, more predictable dose response, and has less severe side effects (50% less side effects).

30
Q

What are some adverse effects associated with heparin?

A

(1) Bleeding
(2) Heparin induced thrombocytopnenia
(3) Osteoporosis (with more than 2 months use)

31
Q

What are the oral anticoagulants?

A

Derivatives of coumarin or indandione

Warfarin is most commonly used.

32
Q

What is the mechanism of warfarin?

A

Warfarin is a vitamin K antagonist.

33
Q

Between warfarin and heparin which one is preferred during pregnancy?

A

Warfarin is teratogenic therefore heparin is preferred because it does not cross the placenta.

34
Q

How is warfarin eliminated?

A

Warfarin is inactivated in the liver and then excreted in the bile.

35
Q

What drug interactions are important for Warfarin?

A

(1) alterations in albumin binding (warfarin is 97% bound
(2) Interactions involving the excretion of warfarin
(3) interactions altering vitamin K absorbtion

36
Q

What is protamine?

A

Protamine is able to inactivate heparin and can be used as an antidote in the event of heparin overdose/excessive bleeding.

37
Q

How can warfarin overdose be managed?

A

Giving vitamin K can overcome the effects of warfarin overdose.

38
Q

How is warfarin therapy managed during surgery?

A

For minor surgery tranexamine acid (an anti-fibrinolytic) can be used as a mouth rinse. However, for major surgery the warfarin must be stopped.

39
Q

What are the ‘New’ anticoagulants?

A

(1) fondaparinux (a factor Xa inhibitor)
(2) Bivalirudin (thrombin inhibitor)
(3) Ximelagraten (thrombin inhibitor

40
Q

What drugs can be used as thrombolytic agents?

A

(1) streptokinase
(2) Acylated plasminogen streptokinase activator complex (APSAC)
(3) tissue plasminogen activator (tPA)
(4) Urokinase type plasminogen activator

41
Q

What are the antiplatelet agents that can be used to fight thrombosis?

A

(1) aspirin (irreversible COX inhibitor)
(2) Dipryidamole (phosphodiesterase inhibitor)
(3) Sulfinpyrazone (competitive inhibitor of COX)
(4) Ticlopidine (is mostly replaced by clopodigrel)
(5) Clopodigrel (ADP receptor antagonist)

42
Q

What are the GPIIb/IIIa inhibitors?

A

(1) abciximab
(2) eptifibatide
(3) tirofiban
They can only be used once.

Essential Hematology (22 decks)

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