Blood: 4.4: Thrombosis Flashcards

1
Q

What is the most common location of a thrombus?

A

DVT (below the knee)

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2
Q

Where can intravascular blood clots occur abnormally?

A

any artery or vein

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3
Q

A thrombus is characterized by _____ and _____, as opposed to a postmortem clot.

A

lines of Zahn; attachment to vessel wall

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4
Q

What is a lines of Zahn?

A

RBC and fibrin streaks in an alternating pattern

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5
Q

What are the 3 major risk factors for thrombosis?

A
  1. disruption of blood flow2. endothelial cell damage3. hypercoagulable state** Virchow’s triad
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6
Q

How does disrupted blood flow contribute to thrombi?

A

stasis or turbulence change normal laminar flow, allowing clots to occur

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7
Q

Name 3 examples of disrupted blood flow.

A
  1. immobilization2. cardiac wall dysfunction (A-fib, MIs)3. aneurysm
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8
Q

How does endothelial damage cause thrombi?

A

endothelium normally protects against coagulation (produces PGI2, NO, heparin-like molecules, TPA, thrombomodulin), but damaged endothelium starts clotting cascade (hides subendothelial collagen and TF)

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9
Q

What does thrombomodulin do?

A

it alters thrombin so that it can activate protein C*protein C then inactiavates factors V and VIII (5 and 8)

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10
Q

What can cause endothelial damage?

A
  1. athrosclerosis2. vasculitis3. high levels of homocystein
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11
Q

Why does serum homocystine increase?

A
  1. vitamin B12 or folate deficiency 2. cystathionine beta synthase (CBS) deficiency
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12
Q

What is cystathionine beta synthase (CBS) deficiency?

A

a genetic deficiency of the enzyme that converts homocystine into cystathionine, characterized by homocystinuria, vessel thrombosis, mental retardation, lens discolorations, and long, slender fingers

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13
Q

What causes hypercoagulable states?

A
  1. excessive procoagulants2. defective anticoagulant proteins* can be inherited or acquired
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14
Q

What is the classic presentation of a hypercoagulable pt?

A

recurrent DVTs or DVTs in young age (can also be in the hepatic and cerebral veins)

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15
Q

_____ and ____ inactivate factors V and VIII.

A

Protein C and Protein S

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16
Q

Which drug’s administration b itself should be avoided in Protein C and Protein S deficient pts?

A

Coumadin/warfarin

17
Q

Coumadin/warfarin blocks the enzyme _____ in the liver.

A

epoxide reductase

18
Q

What is warfarin skin necrosis?

A

thrombi in the skin, causing infarcts and necrosis

19
Q

Which vitamin K dependent factors have the shortest half-lives and will be degraded first?

A

Protein C and Protein S

20
Q

What is Factor V Leiden?

A

genetic mutation of factor V that makes it impossible to be deactivated by protein C and protein S–> excessive factor V activity* the most common INHERITED cause of a hypercoagulable state

21
Q

What is Prothrombin 20210A?

A

a genetic mutation of prothrombin that causes its increased gene expression and promotes thrombus formation

22
Q

What does thrombin do?

A

converts fibrinogen into fibrin for clot formation

23
Q

What does ATIII stand for?

A

Antithrombin III

24
Q

What is ATIII deficiency?

A

lack of molecule that the heparin-like molecules (HLM) can bind to, so there’s increased risk of clot formation

25
What does heparin do to ATIII deficient patients?
it doesn't cause a rise in PTT with standard dosing like it should
26
How does Heparin work?
it binds to and activates antithrombin III (ATIII)
27
What is the tx foor ATIII deficiency?
high dose heparin overlapped with Coumadin/warfarin
28
What drug is associated with hypercoagulablity and why?
oral contraceptives; E induces increased production of coagulation factors