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NYCC Physiopathology > Hemostasis & Thrombosis > Flashcards

Hemostasis & Thrombosis Flashcards

1
Q

what is hemostasis?

A

maintenance of clot-free blood within the vascular system while allowing for the formation of a solid plug of blood under conditions of vessel wall injury

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2
Q

what are the key players in hemostasis?

A

vascular endothelium
platelets
coagulation system

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3
Q

what are the 4 anti-platelet effects of intact endothelium?

A
  1. insulates platelets from subendothelial collagen
  2. prostacyclin (PGI2) synthesis
  3. ADPase synthesis
  4. nitric oxide synthesis
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4
Q

what does prostacyclin (PGI2) do?

A

inhibits platelet aggregation

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5
Q

what does ADPase synthesis do?

A

inhibits platelet aggregation

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6
Q

what does nitric oxide synthesis do?

A

vasodilation and inhibits platelet aggregation

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7
Q

what molecule activates anti-thrombin III?

A

heparin like molecule

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8
Q

what effect does heparin-like molecule have on intact endothelium?

A

anti-coagulant

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9
Q

what does anti-thrombin III do?

A

degrades thrombin

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10
Q

what does tissue plasminogen activator (t-PA) do?

A

converts plasminogen to plasmin

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11
Q

what property does t-PA have?

A

fibrinolytic property of INTACT endothelium

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12
Q

what does plasmin do?

A

degrades fibrin

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13
Q

what are the 4 pro-thrombotic properties of damaged endothelium?

A
  • von willebrand factor synthesis
  • tissue factor synthesis
  • platelet activating factor (PAF)
  • t-PA inhibitor synthesis
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14
Q

what does von Willebrands factor do?

A

essential for platelet adhesion

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15
Q

what does tissue factor do?

A

glycoprotein which activates coagulation system

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16
Q

what are the “bricks” of a thrombus?

A

platelets

17
Q

what are the molecules that are secreted by platelets that cause activation of platelets?

A
  • thromboxane (TXA2)
  • ADP
  • clotting factors V and VIII
  • calcium
18
Q

activated platelets bind to ____

A

vWF

19
Q

activated platelets involved in initiation of the ____

A

coagulation cascade

20
Q

how does a temporary clot become definitive?

A

formation of fibrin from thrombin = fused mass of platelets

21
Q

what is the coagulation system activated by?

A

factor XII or tissue factor

22
Q

what is the end product of coagulation system?

A

fibrin monomers

23
Q

fibrin is the “____” of a thrombus

A

cement

24
Q

what is thrombosis?

A

pathological aggregate of platelets, fibrin and blood cells within the non-interrupted vascular system (where a clot should not be / not a problem here)

25
Q

what is a thrombosis adherent to?

A

vascular endothelium

26
Q

T/F: thrombosis only arise in veins

A

F: arterial or venous circulation

27
Q

what are the 3 predisposing factors to thrombi?

A
  • damage to endothelium
  • alterations in normal blood flow
  • increased coagulability of blood
28
Q

what is another name for the 3 predisposing factors to a thrombi?

A

virchow’s triad

29
Q

what is laminar flow?

A

normal (good) flow in a blood vessel

30
Q

what kind of flow has an obstruction of a blood vessel on either side of it?

A

turbulent flow

31
Q

what does turbulent flow increase the risk of?

A

endothelial damage

32
Q

what are 4 things that can lead to damage of the endothelium?

A
  1. ischemic damage to endocardium
  2. valvular damage
  3. free radical induced damage (radiation, trauma, chemicals, microbes)
  4. hemodynamic stress —-> high BP (more energy hitting the walls
33
Q

name 2 types of alterations in normal blood flow

A

stasis & turbulence

34
Q

what do alterations in normal blood flow cause?

A
  1. physical damage to endothelium
  2. disrupts laminar flow
  3. prevent renal clearance of coagulation proteins
  4. retards flow of anticoagulants to stie of injury
35
Q

what are some examples of causes of increased coagulability of blood?

A
  • genetic defect in anticoagulant proteins or coagulant proteins: Leiden Factor V (inherited hypercoagulability)
  • activated protein C (APC) resistance – Factor V Leiden
  • MTHFR gene (higher risk of heart disease since unable to metabolize homocysteine)
  • neoplasia (release of procoagulants)
  • polycythemia vera (^viscosity)
  • smoking, obesity (soft risks)
36
Q

what causes Activated protein C (APC) resistance — factor V leiden

A

A point mutation in the factor V gene (factor V Leiden) renders it resistant to inhibition by APC

37
Q

_____ action is the most common genetic hypercoagulability disorder and accounts for up to ______ % of patients with venous thrombosis

A

Resistance APC
65%

NYCC Physiopathology (28 decks)

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