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CMOD Week 5 > Clot Formation > Flashcards

Clot Formation Flashcards

1
Q

What are the two main parts of hemostasis?

A

coagulation cascade and platelet activation/aggregation

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2
Q

Damage to endothelium exposes the ECM which causes what to occur?

A

vMF is exposed and undergoes conformational change fro binding to platelets in circulation

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3
Q

How does vMF bind platelets?

A

via GP1b

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4
Q

A defect in vMF results in what disease?

A

Von Willebrand Syndrome

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5
Q

A defect in GP1b results what disease?

A

Bernard Soulier Disease

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6
Q

What happens when platelets bind to vMF on exposed endothelium?

A

they are activated, releasing the contents of their alpha and dense granules

and they undergo conformational change that allows them to bind fibrinogen to begin to aggregate and from a primary (weak) clot

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7
Q

What do platelet alpha granules contain?

A

TxA2, P-selectin, Fibrinogen, Factors V and VIII (main ones)

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8
Q

What do platelet dense granules contain?

A

ADP, Ca2+, histamine, serotonin, epinephrine

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9
Q

What is the significance of Ca2+ being released from dense granules?

A

activation of coagulation factors requires Ca2+

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10
Q

How does endothelial damage stimulate the extrinsic pathway?

A

It exposes TF

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11
Q

How else is TF up-regulated on damage endothelial surfaces?

A

cytokines TNF, IL-1 and bacterial endotoxins up-regulate TF expression

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12
Q

What does the exposed TF do?

A

binds factor VII, making the TF/VIIa complex

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13
Q

What inhibits the TF/VIIa complex formation?

A

tissue-factor pathway inhibitor

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14
Q

What else does TFPI do?

A

inactivates factor Xa

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15
Q

Where is TFPI expressed?

A

healthy endothelial cells only

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16
Q

What does TF/VIIa complex do?

A

activates Xa

17
Q

How is the intrinsic coagulation pathway activated?

A

Kallikrein and ANY negatively charged surface can activated XIIa

18
Q

What does XIIa do?

A

activate XIa, which activates IXa

19
Q

What does activation of every coagulation require?

A

1) phospholipid surface

2) calcium

20
Q

The enzymatic reaction that allows Ca2+ to bind to coagulation factors for activation requires what cofactor?

A

K+ (Coumadin is a drug that inhibits this)

21
Q

What does IXa do?

A

binds with VIIIa to activate more Xa

22
Q

What is VIII activated by once released from platelet alpha granules?

A

thrombin (also activates Va)

23
Q

At this point, the extrinsic and intrinsic pathways combine as Xa. What happens next?

A

Xa and Va convert prothrombin (II) to thrombin (IIa)

24
Q

What inhibits activation/function of VIIIa and Va?

A

Protein C

25
Q

How is Protein C activated?

A

expressed on healthy endothelial cells and is activated via thrombomodulin

26
Q

How does thrombomodulin activate protein C?

A

It changes the function of thrombin to activate Protein C instead of cleaving fibrinogen to fibrin

27
Q

What cofactor does Protein C need to act?

A

Protein S (K+ dependent)

28
Q

What does thrombin do (3 things)?

A

1) activates PAR on the surface of platelets, which with ADP and TxA2 enhance platelet aggregation
2) Converts fibrinogen in the primary clot to fibrin and
3) activates XIIIa to crosslink strands of platelet-fibrin-platelet chains to form the strong secondary clot

29
Q

In the primary clot, how is fibrinogen connected to platelets?

A

via GPIIb/IIIa molecules

30
Q

Defect in GPIIb/IIIa results in what disease?

A

Glanzmann thrombasthenia

31
Q

How is fibrin inactivated to prevent overclotting?

A

plasmin cleaves it

32
Q

How is plasmin activated? (4 things)

A

activated by:

1) factor XIIa
2) tissue plasminogen activator (tPA)
3) Urokinase-like plasminogen activator (uPA) in plasma
4) Streptokinase (bacterial product)

33
Q

Where is tPA produced?

A

healthy endothelial cells

34
Q

When is tPA most active? Why?

A

when attached to fibrin, which ensures that its mostly confined to sites of recent thrombosis

35
Q

How is plasmin inactivated?

A

1) free plasmin rapidly complexes with a2-antiplasmin

2) plasminogen activator inhibitors (PAIs)

36
Q

What are PAIs stabilized by?

A

vitronectin

37
Q

What causes PAIs activation?

A

increased by inflammatory cytokines, especially IFN-y

38
Q

What disease greatly reduces plasma a2-antiplasmin?

A

cirrhosis

39
Q

How would you treat cirrhosis to prevent hemorrhaging?

A

caproic acid

CMOD Week 5 (16 decks)

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