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

Exam 6 - Coagulation Cascade Flashcards

(66 cards)

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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
End point of activation stage
- fibrin clot formation
26
Platelet role in coagulation
- 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
27
Normal platelet count
150,000 - 350,000 / uL
28
Two types of coagulation factors
Proenzymes - become enzymes when activated Procofactors - become cofactors but not actual enzymatic activity
29
Which part of cascade model is no Ca necessary
- interaction of thrombin with fibrinogen
30
Intrinsic pathway
- contact activation / blood itself contacts activation agent - aPTT
31
Extrinsic pathway
- release of TF from damaged tissue | - PT
32
Common pathway
- thrombin production - thrombin cleaves fibrinogen to fibrin - PT
33
Factor XIIa activates
- intrinsic pathway - neutrophils - platelets - fibrinolytic system (starts right away) - form kallikrein (activator of fibrinolysis) - compliment cascade - w/ HMWK forms bradykinin
34
Heparin effect on coagulation
- Amplifies antithrombin (ATIII)...stops coagulation
35
How does XIIIa strengthen fibrin
- protects fibrin from plasmin mediated breakdown
36
Low thrombin [ ] effect on fibrin clot
- lead to loose fibrin plug - fibrin broken down more easily - weak clot...may not form or do job - opposite is true as well
37
Pro's of Cascade model
- How enzymatic steps work and cofactors - showed Ca dependence - development of aptt/ PT
38
Ca chelating anticoagulants
- bind to Ca which stops cascade | - Citrate is example
39
Cons of Cascade model
- 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
3 phases of cell based model
``` 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
Initiation phase step 1
- Cell damage exposes TF on cell - TF binds with VII - VII is converted to VIIa - extrinsic tenase complex forms - TF + VIIa
42
Initiation phase step 2
- 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
Initiation phase step 3
- Prothrombinase complex formed - this complex makes small amount of prime thrombin - factor II into factor IIa - not enough to clot....just recruit platelets
44
Amplification phase
- 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
Amplification phase step 1
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
Amplification phase step 2
- 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
Propagation phase step 1
- XIa converts IX to IXa - IXa attaches to VIIIa - Intrinsic Tenase Complex - Platelet Tenase Complex
48
Propagation phase step 2 and 3
- ITC converts X to Xa - Xa binds to Va to make PTC - Large number of PTC makes thrombin burst
49
Clot formation
- 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
Vascular constriction
- more prominent in crushing injuries | - constriction of smooth muscle (smaller vessels)
51
Platelet adhesion problem
- 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
Platelet adhesion
- 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
Platelet activation
- loses discoid shape - GPIb + vWF - GPIIb/IIIa + vWF (holds platelet) - GPIa/IIa + collagen (holds platelet) - GPIV + collagen (signaling)
54
Goals of platelet activation
- recruit more platelets - bind platelets to each other to make matrix - fibrin formation - protect clot from fibrinolysis
55
Platelet recruitment
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
Formation of platelet plug
- 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
Termination players
- TFPI - PC - PS - ATIII
58
TFPI
- made of TF/VIIa/Xa/TFPI | - inhibits priming dose of thrombin
59
PC and PS
- 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
ATIII
- inhibits thrombin | - inhibits 9a to 12a
61
Fibrinolysis
- plasmin signals start of this phase
62
Plasmin
- formed from plasminogen - actively breaks down clots by cleaving fibrin polymers - cleaved fibrin produced more fibrin degradation products
63
Endogenous anticoagulants
- 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
Bleeding and CPB
- bad outcomes - more cost - more infection - more blood products
65
CPB and coagulation
- activates intrinsic/extrinsic coagulation pathways - from suction / negatively charged surface - activates neutrophils / monocytes - surgery exposes subendothelium - activates platelets - activates endothelial cells
66
Five causes of bleeding post-op
- surgical leak - insufficient fibrin formation - insufficient clot integrity - insufficient clot adhesion - fibrinolysis

562 - Perfusion Technology II (9 decks)

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