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Biochemistry S2 > CR II - Coagulation > Flashcards

CR II - Coagulation Flashcards

1
Q

What are 4 major components that interact to promote and inhibit clot formation? What do each do?

A

Endothelial cells - inhibit clot formation
Sub endothelial tissues - form clots when in contact with platelets
Platelets - activated, release factors for activation of coagulation - soft plug
Clotting factors - in plasma, platelets, and subendothelial activate to form hard clot

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2
Q

What 2 things do endothelial cells produce/express to inhibit coagulation? What 1 thing does it produce to inhibit platelet activation? What 1 thing does it produce to stimulate clot dissolution?

A

Inhibit coagulation - heparin sulfate proteoglycan and thrombomodulin
Inhibit platelet activation - prostacyclin PGI2
Stimulate clot dissolution - tissue plasminogen activator (tPA)

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3
Q

What are the three phases of hemostasis? Do they occur in sequence or simultaneously?

A

Pro-coagulation
Anti-coagulation
Fibrinolysis
Simultaneously

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4
Q

What are two receptors expressed by platelets to directly and indirectly bind to collagen?

A

GPIb/IX/V - indirect, binds to vWF which then binds to collagen
GPIa/IIa - direct, binds directly to collagen

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5
Q

What 6 additional compounds that are released in hemostasis? What do each do?

A

ADP - stimulates further platelet activation by binds to G-Protein coupled P2Y receptors
Serotonin - vasoconstrictor (around damaged endothelium)
Fibrinogen
Factors V, VII, and Ca
VWF
Platelet derived growth factor (PDGF) - for improved wound healing
Thrombocytes A2 (TXA2) - stimulates further platelet activation

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6
Q

Which factor overcomes the excretion by the endothelium to prevent coagulation?

A

Thromboxane A2

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7
Q

What membrane receptor on platelets is the most abundant? Once the platelet is activated, what does this receptor bind? Aggregates what?

A

GPIIb/IIIa
Binds fibrinogen
Aggregates activated platelets

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8
Q

How to platelets change once they are bound to collagen? What do they form?

A

Change shape

Form physical plug

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9
Q

How does the platelet surface change to provide place for coagulation?

A

Phosphatidylserine (PS) moves from inner leaflet to outer leaflet

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10
Q

What pathway initiates coagulation? When what is exposed to plasma?

A

Extrinsic pathway

When tissue factor is exposed to plasma

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11
Q

Where is tissue factor found? What does it bind to to initiate the extrinsic pathway? What is required to do this?

A

Transmembrane in subendothelium
Finds to FVII
Only in presence of Ca2+

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12
Q

After FVII is activated by binding to tissue factor, what two things is it further activated by?

A

FXa or thrombin

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13
Q

What complex is formed what tissue factor binds to FVII with CA? What else is this called? What does it activate?

A

tissuefactor-FVIIa-Ca complex
X-are complex
Activates FX to FXa and FIX to FIXa

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14
Q

Why is it ok that FVIIa has a long half-life?

A

Because it is only active when bound to tissue factor

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15
Q

What is the first step in the final common pathway?

A

Formation of FXa from FX

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16
Q

What forms a platelet membrane bound complex with FXa? What does this complex do? What is needed?

A

FV (from platelets)
Cleaves prothrombin to thrombin
Ca is required for prothrombin to bind to membrane

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17
Q

What are two things that thrombin does?

A

Converts fibrinogen to fibrin monomers

Promotes further coagulation by activating factors in intrinsic, extrinsic, and common pathways

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18
Q

What 5 factors can thrombin activate?

A

FVIII and XI - intrinsic
FV and FXIII - common
FVII of extrinsic

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19
Q

What pathway is coagulation initiated through?

A

Intrinsic pathway

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20
Q

What is required for initiation of the intrinsic pathway?

A

Exposure to anionic surface

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21
Q

Where do proteins of the intrinsic pathway come from? Which binds first to anionic surface? What does it undergo?

A

Plasma

FXII - undergoes conformational change to increase activity

22
Q

What two factors are brought close to FXII by complexing with HMWK? Where does HMWK also bind?

A

FXI and prekallikrein

HMWK also binds to anionic surfaces

23
Q

What activates prekallikrein to kallikrein? What are the next 4 steps in the intrinsic pathway?

A 
FXII
Kallikrein activates FXII to TXIIa
FXIIa activates FXI to FXIa
FXIa activates FIX to FIXa
FIXa and FVIIa activates FX to FXa (Ca dependent)
24
Q

What protects FVIII from proteolytic destruction prematurely?

A

Bound to vWF in plasma

25
Q

What of fibrinogen prevents its aggregation? What remedies this allowing formation of soft clot?

A

Amino termini of central globular domain

Thrombin cleaves amino termini, releasing fibrinopeptides allowing aggregation of to form soft clot

26
Q

What factor acts on fibrin to form hard clot? What is it activated by? What is it classified as? What two residues on fibrin does it link? With what bond?

A 
FXIIIa
Activated by thrombin
Classified as transflutaminase
Transamidination between glutaminyl and lysyl residues on two different fibrin
Covalent linkage
27
Q

What are the 7 enzymes or factors involved in anti-coagulation? Which two are Vitamin K dependent?

A 
Antithrombin
Thrombomodulin
Protein C - vit K dependent
Protein S - vit K dependent
Tissue factor pathway inhibitor
Other serpins
NO
28
Q

Where is antithrombin synthesized? What 5 things does it inactivate? What greatly enhances its activity?

A

Synthesized in liver
Inactivated thrombin, FIXa, FX, FXIa, and FXIIa
Glycoasminoglycans - heparin and heparan sulfate

29
Q

What is thrombomodulin? Where is it found? What binds, forming a complex to reduce activity? What activity does this complex activate?

A

Plasma membrane receptor protein
Endothelial cells
Thrombin binds, reducing activity of thrombin to bind fibrinogen
Increases activity of protein C

30
Q

Where is Protein C synthesized? Where is then found? What activates it? What does it then form a complex with?

A

Liver
Plasma
Activated by thrombin-thrombomodulin complex
forms complex with Protein S (APC)

31
Q

Where does the APC complex bind? What does it depend on? What two factors does it inactivate?

A

APC binds to surface of platelet
Depends on Ca
Inactivates FVa and FVIIIa

32
Q

What protein, bound to lipoproteins, circulates in blood and binds/inactivates tissuefactor-FVIIa-Ca_FXa complex?

A

Tissue factor pathway inhibitor

33
Q

What are serpins? Where are they found? What do they bind? What are three examples?

A

Serine Protease inhibitors
Circulate in plasma
Bind to proteases (coagulation factors) inactivating them
Anti-thrombin, a-macroglobulin, a-antitrypsin

34
Q

Besides vasodialation, what does NO do?

A

Inhibits platelet adhesion and aggregation

35
Q

What are three major compounds that activate plasminogen to plasmin?

A

Tissue plasminogen activator
Urokinase
Streptokinase

36
Q

In liquid phase of blood, what rapidly inactivates plasmin?

A

alpha-antiplasmin

37
Q

What must tPA be bound to in order to be active? What is excess tPA activity prevented/inhibited by?

A

Fibrin

Inhibited by PAI-I

38
Q

What activates urokinase?

A

Conformationally activated FXII

39
Q

How does streptokinase activate plasminogen?

A

By confirmational change

40
Q

What are the 6 vitamin K dependent factors? What do they contain which is required for Ca binding? Where is this created? What does this process depend on?

A

Prothrombin (II), FVII, FIX, FX, protein C and protein S
Gamma-carboxyglutamyl residues
Post-translationally in liver
Vitamin K dependent process

41
Q

What disorder prolongs bleeding time?

A

Platelet disorders

42
Q

When will activated partial thromboplastin time (aPTT) be prolonged?

A

Deficiency in either intrinsic or common pathway

43
Q

What is added to citrated platelet-poor plasma for aPTT? For Prothrombin time?

A

aPTT - kaolin (clay providing anionic surface), phospholipids, and excess Ca
Prothrombin time - tissue factor-containing extract and exces Ca

44
Q

When will prothrombin time be prolonged?

A

Extrinsic and common

45
Q

What two things cause prolonged thrombin time?

A

Persons treated with heparin or who have fibrogen deficiency

46
Q

What two deficiencies cause hemophilia? Which is more common? Are both genetic?

A

Hemophilia A - deficiency FVIII - more common
Hemophilia B - deficient FIX
Both x-linked recessive

47
Q

What deficiency may also be associated with von Willebrand disease?

A

FVIII deficiency

48
Q

Is von Willebrand disease consistent? Common? What is treatment?

A

Highly variable
Very common
Replacement therapy

49
Q

What is deficient in Bernard-Suulier disease? How does it differ from von Willebrand disease?

A

GPIb/IX/V receptors deficient

FVIII not affected

50
Q

What is characterized by Factor V Leiden?

A

Mutation in FV normal cleavage site

FVa inactivation much slower leading to hyper coagulable state

Biochemistry S2 (13 decks)

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