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562 - Perfusion Technology II > Exam 6 - Coagulation Cascade > Flashcards

Exam 6 - Coagulation Cascade Flashcards

1
Q

Factor I

A

Fibrinogen

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2
Q

Factor II

A

Prothrombin

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3
Q

Factor III

A

Tissue thromboplastin

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4
Q

Factor IV

A

Calcium

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5
Q

Factor V

A

Proaccelerin

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6
Q

Factor VII

A

Proconvertin

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7
Q

Factor VIII

A

Antihemophilic factor A

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8
Q

Factor IX

A

Plasma thromboplastin component

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9
Q

Factor X

A

Stuart factor

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10
Q

Factor XI

A

Plasma thromboplastin antecedent

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11
Q

Factor XII

A

Hageman factor

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12
Q

Factor XIII

A

Fibrin stabilizing factor

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13
Q

PC

A

Protein C

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14
Q

PS

A

Protein S

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15
Q

HMWK

A

High molecular weight kininogen

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16
Q

TF

A

Tissue factor (thromboplastin)

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17
Q

Prothrombinase complex

A

Xa bound to Va+Ca on PL

Xa + Va

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18
Q

Extrinsic tenase complex

A

VIIa + TF

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19
Q

Intrinsic Tenase Complex

A
  • Platelet tenase complex

- IXa + VIIIa

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20
Q

Hemostasis

A
  • circulatory homeostasis

- keep blood liquid…but stop from bleeding

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21
Q

How hemostasis is maintained

A 
Anticoagulant factors:
- from endothelial cells
Procoagulant factors:
- platelets 
- plasma proteins in inactive states (zymogens...most are)
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22
Q

Arterial circulation

A
  • high flow, high pressure
  • smaller vessels
  • platelets are big player
  • anti-platelet agents used to treat thrombosis
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23
Q

Venous circulation

A
  • low flow, low pressure
  • bigger vessels
  • rate of thrombin formation big player
  • antithrombin agents for DVT
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24
Q

What happens when arterial blood vessel damaged

A
  • constriction
  • platelet adhesion
  • platelet activation (plug forms)
  • coagulation and fibrin clot formation
  • clot retraction
  • fibrinolytic cascade
  • vessel repair
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25
Q

End point of activation stage

A
  • fibrin clot formation
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26
Q

Platelet role in coagulation

A
  • needed for quick clot formation
  • provide surface to take place on
  • receptor site for coagulation factors
  • release some factors
  • not just # important…but need to be activated at site of injury
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27
Q

Normal platelet count

A

150,000 - 350,000 / uL

28
Q

Two types of coagulation factors

A

Proenzymes
- become enzymes when activated
Procofactors
- become cofactors but not actual enzymatic activity

29
Q

Which part of cascade model is no Ca necessary

A
  • interaction of thrombin with fibrinogen
30
Q

Intrinsic pathway

A
  • contact activation / blood itself contacts activation agent
  • aPTT
31
Q

Extrinsic pathway

A
  • release of TF from damaged tissue

- PT

32
Q

Common pathway

A
  • thrombin production
  • thrombin cleaves fibrinogen to fibrin
  • PT
33
Q

Factor XIIa activates

A
  • intrinsic pathway
  • neutrophils
  • platelets
  • fibrinolytic system (starts right away)
    • form kallikrein (activator of fibrinolysis)
  • compliment cascade
  • w/ HMWK forms bradykinin
34
Q

Heparin effect on coagulation

A
  • Amplifies antithrombin (ATIII)…stops coagulation
35
Q

How does XIIIa strengthen fibrin

A
  • protects fibrin from plasmin mediated breakdown
36
Q

Low thrombin [ ] effect on fibrin clot

A
  • lead to loose fibrin plug
  • fibrin broken down more easily
  • weak clot…may not form or do job
  • opposite is true as well
37
Q

Pro’s of Cascade model

A
  • How enzymatic steps work and cofactors
  • showed Ca dependence
  • development of aptt/ PT
38
Q

Ca chelating anticoagulants

A
  • bind to Ca which stops cascade

- Citrate is example

39
Q

Cons of Cascade model

A
  • Only works in-vitro
  • only applies if blood is NOT moving and not interacting with other cells / linings
  • Shows intrinsic and extrinsic can activate factor X separately
    • in vivo they can’t (extrinsic needed)
40
Q

3 phases of cell based model

A 
initiation phase
- occurs on TF bearing cells
amplification phase
- platelets and cofactors activated
- recruiting phase 
propagation phase
- thrombin burst
- clot formation 
- takes place on platelets
41
Q

Initiation phase step 1

A
  • Cell damage exposes TF on cell
  • TF binds with VII
  • VII is converted to VIIa
    • extrinsic tenase complex forms
    • TF + VIIa
42
Q

Initiation phase step 2

A
  • Extrinsic tenase complex converts:
    • IX to IXa
    • X to Xa
  • IXa inhibited by TFPI and ATIII
    • Tissue factor pathway inhibitor
  • If ACTIVATED platelets close…IXa (w/ help of VIIIa) will convert more X to Xa
43
Q

Initiation phase step 3

A
  • Prothrombinase complex formed
  • this complex makes small amount of prime thrombin
    • factor II into factor IIa
    • not enough to clot….just recruit platelets
44
Q

Amplification phase

A
  • Priming IIa is signal to start this phase
  • purpose is to recruit and activate platelets
  • still no clot formation
  • for clot to form…injury must allow big proteins of amplification/propagation to move out of vessel into tissue where the TF bearing cells are located
45
Q

Amplification phase step 1

A

Factor IIa (thrombin) from initiation is busy:

  • activates platelets….very important
  • V to Va
  • Splits VIII+vWF into VIII and VWF
  • XI to XIa
46
Q

Amplification phase step 2

A
  • IIa binds and activates platelet
    • platelet shape change
    • new shape promotes binding
    • release of granules for more platelet activation
  • Va / VIIIa / XIa binds to activated platelet
  • IXa and VIIIa form Intrinsic Tenase Complex
47
Q

Propagation phase step 1

A
  • XIa converts IX to IXa
  • IXa attaches to VIIIa
    • Intrinsic Tenase Complex
    • Platelet Tenase Complex
48
Q

Propagation phase step 2 and 3

A
  • ITC converts X to Xa
  • Xa binds to Va to make PTC
  • Large number of PTC makes thrombin burst
49
Q

Clot formation

A
  • happens after thrombin burst
  • fibrin clot forms
  • majority of thrombin comes AFTER fibrin clot formed
    • thrombin also converts XIII to XIIIa to make clot stronger
    • additional thrombin is just to make clot stronger
50
Q

Vascular constriction

A
  • more prominent in crushing injuries

- constriction of smooth muscle (smaller vessels)

51
Q

Platelet adhesion problem

A
  • area of injury has high shear stress….so low velocity
    • hard for platelets to stick
    • BUT coaxial migration pushes more platelets to outer vessel
    • platelets pushed out to side by larger proteins in middle
52
Q

Platelet adhesion

A
  • must happen fast
    Platelet binds to:
  • vWF: held by collagen
  • GPIb: on platelet…binds to vWF…slows down platelet at injury site
  • over time platelet slows enough to actually stop
  • interaction of GPIb and vWF causes transmembrane signaling
  • signaling AND shear stress activates platelets at injury site
53
Q

Platelet activation

A
  • loses discoid shape
  • GPIb + vWF
  • GPIIb/IIIa + vWF (holds platelet)
  • GPIa/IIa + collagen (holds platelet)
  • GPIV + collagen (signaling)
54
Q

Goals of platelet activation

A
  • recruit more platelets
  • bind platelets to each other to make matrix
  • fibrin formation
  • protect clot from fibrinolysis
55
Q

Platelet recruitment

A

Platelets release 3 agonists:
- Thromboxane (TXA2): vasoconstrictor, made in platelet, released by platelet…aspirin prevents formation of this…recruitment down

  • Serotonin: released from granules, vasoconstrictor
  • ADP: from granules, no known role
56
Q

Formation of platelet plug

A
  • GPIIb/IIIa changes via calcium
  • complex can bind to vWF or fibrinogen in tight matrix to form plug 1st
  • clot formed following plug formation
57
Q

Termination players

A
  • TFPI
  • PC
  • PS
  • ATIII
58
Q

TFPI

A
  • made of TF/VIIa/Xa/TFPI

- inhibits priming dose of thrombin

59
Q

PC and PS

A
  • inactivate Va / VIIIa
  • vitamin K dependent
  • Va needed for PTC and platelet activation
  • VIIIa needed for Xa formation
  • PC also activated by thrombin…negative feedback
  • PC accelerated by PS…positive feedback
60
Q

ATIII

A
  • inhibits thrombin

- inhibits 9a to 12a

61
Q

Fibrinolysis

A
  • plasmin signals start of this phase
62
Q

Plasmin

A
  • formed from plasminogen
  • actively breaks down clots by cleaving fibrin polymers
  • cleaved fibrin produced more fibrin degradation products
63
Q

Endogenous anticoagulants

A
  • keeps blood liquid
  • need INTACT endocellular barrier
    • release NO and PGI2…prevent platelet adhesion/aggregation
    • release ADPase….limits recruitment of platelets
  • all overridden by high platelet count at injury site
64
Q

Bleeding and CPB

A
  • bad outcomes
  • more cost
  • more infection
  • more blood products
65
Q

CPB and coagulation

A
  • activates intrinsic/extrinsic coagulation pathways
    • from suction / negatively charged surface
  • activates neutrophils / monocytes
  • surgery exposes subendothelium
  • activates platelets
  • activates endothelial cells
66
Q

Five causes of bleeding post-op

A
  • surgical leak
  • insufficient fibrin formation
  • insufficient clot integrity
  • insufficient clot adhesion
  • fibrinolysis

562 - Perfusion Technology II (9 decks)

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