EXAM #1: THROMBOSIS Flashcards

1
Q

What is the definition of thrombosis?

A

Pathological blood clotting in an uninjured blood vessel or exaggerated clotting in response to minimal injury

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2
Q

Outline Virchow’s Triad.

A

These are the major factors that predispose one to thrombosis:

1) Endothelial injury
2) Blood stasis or turbulence to blood flow
3) Blood hypercoaguability

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3
Q

What are the anti-platelet effects of the endothelium?

A
  • Non-activated platelets do NOT adhere to the endothelium

- PGI2 and NO produced by the endothelium prevent platelet activation

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4
Q

What are the anti-coagulant properties of the endothelium?

A
  • Heparin like molecule activates anti-thrombin III

- Thrombomodulin binds thrombin to activate Protein C

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5
Q

What are the fibrinolytic properties of the endothelium?

A

Endothelium synthesizes t-PA

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6
Q

What are the prothrombic properties of the endothelium?

A
  • vWF
  • TF
  • Plasminogen activator inhibitors (PAI)
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7
Q

Describe the mechanism of action of ASA.

A

ASA prevents platelet activation and release

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8
Q

List the contents of the dense granules.

A
ATP 
ADP 
Ca++ 
Histamine 
Epi
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9
Q

List the contents of the alpha granules.

A
P-selectin 
Fibrinogen 
Fibronectin 
Factor V 
VIII 
PDGF 
TGF-a
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10
Q

Outline the process that leads to the development of the primary platelet plug.

A

1) vWF and Gp1b causes platelet adherence
2) Ca++ mediates secretion of granules
3) GpIIb/IIIa binds fibrin

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11
Q

What is a major predisposing factor for thrombosis? Why?

A

Endothelial dysfuction–loss of endothelium will expose the ECM and activate platelets and thrombosis

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12
Q

What is the effect of blood turbulence on the endothelium?

A

Turbulence enhances endothelial injury

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13
Q

What is the effect of stasis on the endothelium?

A

Enhances venous thrombosis

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14
Q

What are the combined effects of blood stasis and turbulence of flow?

A
  • Platelets are brought close to endothelium
  • Clotting factors accumualte
  • Clotting factor inhibitors are blocked
  • Endothelial activation occurs
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15
Q

What happens to vWF under shear stress?

A

Unfolding i.e. the faster blood flows, the STICKIER it gets

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16
Q

What are the primary causes of hypercoaguability?

A
  • Factor V Leiden
  • Antithrombin III deficiency
  • Protein C/S deficiency
  • Prothrombin gene mutation
17
Q

What are the secondary causes of hypercoaguability?

A
  • Anti-phospholipid Syndrome
  • Lupus
  • Stasis
  • Cancer
  • Nephrotic syndrome
  • Contraceptive pills
  • Smoking
18
Q

What is Heparin-Induced Thrombocytopenia (HIT)?

A
  • Heparin therapy

- Heparin antibodies binding platelets and activate them

19
Q

What is Antiphospholipid Syndrome?

A

Antibodies to phospholipids

20
Q

What is the difference between a superficial and deep venous thrombosis?

A

Superficial= rarely embolize but can be quite painful

Deep= more frequently embolize

**Note that only 50% of patients will have a symptomatic DVT b/c of collateral circulation

21
Q

What is DIC?

A

Disseminated Intravascular Coagulation

  • Sudden fibrin thrombi in microcirculation
  • Leads to circulatory insufficiency

Paradoxically CONSUMES platelets and clotting factors, increasing risk of bleeding

22
Q

Outline the fates of a thrombus.

A

1) Propagation
2) Embolization
3) Lysis
4) Organization and recanalization

23
Q

What is the second most common medical complication?

A

DVT

24
Q

What is the most common cause of preventable death in hospital?

A

PE

25
Q

What are the risks and complications associated with a VTE?

A
  • Increased risk for recurrent VTE

- Post-thrombotic syndrome

26
Q

What are the different types of PEs?

A

1) Small= silent
2) Medium= pulmonary infarct with acute respiratory and cardiac symptoms
3) Large= right heart failure and collapse
4) Massive= sudden death

27
Q

What is a paradoxical embolus?

A

Venous embolus passing the arterial circulation through a septal defect, causing an arterial embolism

28
Q

What tissue is the most vulnerable to hypoxia?

A

Neurons (can only handle 3-4 minutes of anoxia)

29
Q

How much is the relative risk of thrombophlia increased with a homozygous Factor V Leiden Deficiency?

A

80x

**vs. 7x in heterozygous

30
Q

How much does oral contraception increase the risk for thrombosis?

A

3.7x

31
Q

How much does Factor V Leiden Deficiency + oral contraception increase the risk for thrombosis?

A

34.7x

32
Q

How do you evaluate the clotting state of a patient?

A
  • PT, PTT, TT, Fibrinogen

- Assess clotting factors

33
Q

When do you further evaluate a patient with a clot of a patient that presents with a family history of clotting?

A
  • Young patient
  • Family history
  • Thrombosis in absence of known risk factors
  • Recurrent miscarriage
  • Warfarin-induced skin necrosis
  • Neonatal pupura fulminans
34
Q

What is a factor that you would normally further evaluate, which you no longer do?

A

MTHFR