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Liz's Hemostasis/Coagulation > Thrombophilia and Anticoagulant Therapy > Flashcards

Thrombophilia and Anticoagulant Therapy Flashcards

1
Q

Discuss the mechanism by which coagulation is inhibited by tissue factor pathway inhibitor (TFPI)

A
  • Inhibits the TF pathway by inactivating Factor VIIa

- Due to the action of TFPI: TF-VIIa is short lived and coagulation amplification occurs primarily through XI

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2
Q

Origin of Protein C (and Protein S)

A

Synthesized in the liver

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3
Q

What are Protein C and S dependent upon?

A

Vitamin K

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4
Q

What is the principle of Protein C and S by which coagulation is inhibited and affected factors?

A

It inactivates Va and VIIIa and may cause recurrent thromboses (blood clot)

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5
Q

State the mutation that is responsible for the most commonly inherited form of thrombophilia

A

Activated Protein C resistance (APCR) → called Factor V Leiden mutation

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6
Q

Origin of antithrombin

A

Liver

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7
Q

Is antithrombin dependent upon Vitamin K?

A

No

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8
Q

Principle of antithrombin (AT) by which coagulation is inhibited, including affected factors

A
  • Serine protease inhibitor (SERPIN)

- Irreversibly binds and neutralizes the serine proteases `in the intrinsic pathways: XIIa, XIa, IXa, Xa, thrombin (IIa)

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9
Q

In the antithrombin, when no heparin is present, AT’s binding w/ the serine proteases is a ____ reaction

A

Slow, progressive

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10
Q

When either endothelial cell heparan or exogenously administered ____ is present, ____ binding w/ the serine proteases is ____ and enhanced 1,000-fold!!

A

Heparin is present; AT’s binding; immediate

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11
Q

The effect of deficiency states of antithrombin (AT) and protein C (protein S)

A

May cause recurrent thromboses

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12
Q

Eight factors that predispose a person to thrombosis

A
  • Age
  • Hereditary
  • Immobilization/stasis
  • Smoking
  • Malignancy
  • Injury to vessels (trauma, surgery)
  • Elevated estrogens (low protein S, C, AT)
  • Inflammation
  • Antiphospholipid syndrome
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13
Q

Three types of thomboses

A
  • Arterial thromboses
  • Microcirculatory (TTP, HUS, DIC)
  • Venous thromboses
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14
Q

What is the process by which arterial thrombosis are formed?

A

Result of a disease process which causes major damage in a vessel wall (myocardial infarction, arteriosclerosis)

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15
Q

Arterial thrombosis

- Major component

A

Platelets

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16
Q

Arterial thrombosis

- Treatment

A

Anti-platelet drugs (aspirin, plavix)

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17
Q

Process by which venous thrombosis are formed?

A

Result of a major stasis in blood flow (DVT, pulmonary embolus)

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18
Q

Venous thrombosis

- Major component

A

Fibrin

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19
Q

Venous thrombosis

- Treatment

A

Antifibrin drugs (heparin, coumadin)

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20
Q

Defined as a predisposition of thrombosis secondary to a congenital or acquired disorder

A

Thrombophilia

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21
Q

Defined as the inappropriate formation of platelet or fibrin clots that obstruct vessels

A

Thrombosis

22
Q

Defined as any foreign object in the bloodstream such as air, bullet, clot

A

Embolus

23
Q

Four types of anticoagulant therapy

A
  • Standard unfractionated heparin (UFH)
  • Low molecular weight heparin (LMWH)
  • Coumadin drugs
  • Thrombolytic agents (clot busters)
24
Q

Standard unfractionated heparin (UFH)

- Mechanism of action

A

Heparin by itself is NOT and anticoagulant must complex w/ AT and ATP is called the “heparin co-factor”

25
Q

Standard unfractionated heparin (UFH)

- Indication for therapy

A

Treatment of thrombosis to prevent propagation

26
Q

Standard unfractionated heparin (UFH)

- Administration

A

IV or subcutaneously (SQ)

27
Q

Standard unfractionated heparin (UFH)

- Monitoring

A

APTT

  • Target for therapy
  • Prophylaxis
  • Daily platelet counts to detect HIT
28
Q

Standard unfractionated heparin (UFH)

- Overdose

A

Treat w/ protamine sulfate

29
Q

Low molecular weight heparin (LMWH)

- Mechanism of action

A

Increases the inhibitor effect of AT on thrombin and Xa (mainly Xa)

30
Q

Also known as Lovenox

A

Low molecular weight heparin (LMWH)

31
Q

Low molecular weight heparin (LMWH)

- Administration

A

SQ

32
Q

Low molecular weight heparin (LMWH)

- Indication for therapy

A

Treatment of thrombosis to prevent propagation; not as commonly used but great for those needing to go home on heparin

33
Q

Low molecular weight heparin (LMWH)

- Monitoring

A

Anti-Xa heparin assay (APTT is insensitive)

34
Q

Why is monitoring Low molecular weight heparin (LMWH) necessary?

A

For infants, children, obese or underweight patients, those w/ renal disease, or unexpected bleeding

35
Q

Which brand is most common for long-term anticoagulant therapy?

A

Coumadin

36
Q

Which brand is the oldest brand name for long-term anticoagulant therapy

A

Warfarin

37
Q

Coumadin

- Mechanism of action

A

Coumadin blocks the action of vitamin K which is needed for the synthesis of the vitamin K dependent factors. Therefore, slowing thrombin formation

38
Q

What are the vitamin K dependent factors?

A

Prothrombin group (II, VII, IX, X)

39
Q

Coumadin

- Administration

A

Oral

40
Q

Coumadin

- Delayed reaction or immediate reaction?

A

Delayed reaction (3-5 days)

41
Q

Coumadin

- Indication for therapy

A

Treatment of thrombosis to prevent propagation; prevention of thromboembolic disease in thrombophilia, mechanical heart valves, and high risk surgery.

42
Q

Coumadin

- Monitoring

A

PT and INR

43
Q

Coumadin

- Overdose

A

Treat by giving vitamin K and FFP if major bleeding

44
Q

Standard Unfractionated Heparin (UFH)

- Immediate or delayed reaction?

A

Immediate reaction

45
Q

List sources of vitamin K

A
  • Diet: green leafy vegetables, fish, and liver

- Normal gut flora: E. coli, B. fragilis

46
Q

Three situations in which vitamin K deficiency may occur

A
  • Poor diet
  • Long-term antibiotic therapy
  • Newborns
47
Q

Vitamin K makes the prothrombin factors functional by ____

A

By adding a 2nd carboxyl group on the γ carbon. In vitamin K deficiency or in the presence of a vitamin K antagonist, these factors are released from the liver without the γ-carboxylation rendering them nonfunctional

48
Q 
Thrombolytic agents (clot busters)
- Mechanism of action
A

Indiscriminately induce in vivo fibrinolysis by activating plasminogen to plasmin; not only get rid of bad clots but good clots too

49
Q

Types of thrombolytic agents

A
  • Tissue plasminogen activator (TPA)
  • Streptokinase
  • Urokinase
50
Q

Why is TPA considered the best/safest clot buster?

A

B/c it will NOT activate circulating (free) plasminogen…only fibrin bound

51
Q

When is the therapeutic agent TPA used?

A
  • Life threatening thromboses

- Must be given w/in 4-6 hours of onset

Liz's Hemostasis/Coagulation (10 decks)

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