Pathoma- thrombosis

Question 1

What is the most common location of a thrombus?

Answer 1

DVT (below the knee)

Question 2

Where can intravascular blood clots occur abnormally?

Answer 2

any artery or vein

Question 3

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

Answer 3

lines of Zahn; attachment to vessel wall

Question 4

What is a lines of Zahn?

Answer 4

RBC and fibrin streaks in an alternating pattern

Question 5

What are the 3 major risk factors for thrombosis?

Answer 5

1. disruption of blood flow
2. endothelial cell damage
3. hypercoagulable state

** Virchow’s triad

Question 6

How does disrupted blood flow contribute to thrombi?

Answer 6

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

Question 7

Name 3 examples of disrupted blood flow.

Answer 7

1. immobilization
2. cardiac wall dysfunction (A-fib, MIs)
3. aneurysm

Question 8

How does endothelial damage cause thrombi?

Answer 8

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

Question 9

What does thrombomodulin do?

Answer 9

it alters thrombin so that it can activate protein C

*protein C then inactiavates factors V and VIII (5 and 8)

Question 10

What can cause endothelial damage?

Answer 10

1. athrosclerosis
2. vasculitis
3. high levels of homocystein

Question 11

Why does serum homocystine increase?

Answer 11

1. vitamin B12 or folate deficiency

2. cystathionine beta synthase (CBS) deficiency

Question 12

What is cystathionine beta synthase (CBS) deficiency?

Answer 12

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

Question 13

What causes hypercoagulable states?

Answer 13

1. excessive procoagulants
2. defective anticoagulant proteins

• can be inherited or acquired

Question 14

What is the classic presentation of a hypercoagulable pt?

Answer 14

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

Question 15

_____ and ____ inactivate factors V and VIII.

Answer 15

Protein C and Protein S

Question 16

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

Answer 16

Coumadin/warfarin

Question 17

Coumadin/warfarin blocks the enzyme _____ in the liver.

Answer 17

epoxide reductase

Question 18

What is warfarin skin necrosis?

Answer 18

thrombi in the skin, causing infarcts and necrosis

Question 19

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

Answer 19

Protein C and Protein S

Question 20

What is Factor V Leiden?

Answer 20

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

Question 21

What is Prothrombin 20210A?

Answer 21

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

Question 22

What does thrombin do?

Answer 22

converts fibrinogen into fibrin for clot formation

Question 23

What does ATIII stand for?

Answer 23

Antithrombin III

Question 24

What is ATIII deficiency?

Answer 24

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

Question 25

What does heparin do to ATIII deficient patients?

Answer 25

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

Question 26

How does Heparin work?

Answer 26

it binds to and activates antithrombin III (ATIII)

Question 27

What is the tx foor ATIII deficiency?

Answer 27

high dose heparin overlapped with Coumadin/warfarin

Question 28

What drug is associated with hypercoagulablity and why?

Answer 28

oral contraceptives; E induces increased production of coagulation factors