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
Q

What does heparin do to ATIII deficient patients?

A

it doesn’t cause a rise in PTT with standard dosing like it should

26
Q

How does Heparin work?

A

it binds to and activates antithrombin III (ATIII)

27
Q

What is the tx foor ATIII deficiency?

A

high dose heparin overlapped with Coumadin/warfarin

28
Q

What drug is associated with hypercoagulablity and why?

A

oral contraceptives; E induces increased production of coagulation factors