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Perf Tech > coagulation review > Flashcards

coagulation review Flashcards

1
Q

circulatory homeostasis is maintained

A

preservation of blood fluidity and ability to seal off bleeding

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2
Q

anticoagulant factors are released by

A

endothelial cells (prostacylcin ,vascular plasminogen activator) tend to be released from lining

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3
Q

procoagulant factors

A

platelets, plasma proteins-inactive state (zymogen) tend to be released when lining is disrupted

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4
Q

most significant event in vivo to initiate coag.

A

Factor VIIa/TF is the most significant event to initiate coagulation

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5
Q

phase1 :initiation activation of factor VII

A

 Vascular damage exposes TF (a membrane-
bound protein) to plasma
 TF is both a receptor and cofactor for FVII
 When the zymogen FVII binds TF it converts to FVIIa (we don’t know exactly why) and forms the FVIIa/TF complex

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6
Q

PHASE 1 INITIATION : The FVIIa/TF complex activates

A

the FIX and FX zymogens (what are those again?)
 FXa formed on the TF-bearing cell interacts with cofactor Va to form a prothrombinase complex and (very importantly) generates a very small amount of “priming” thrombin on the surface of TF-bearing cells.
 FXa remains on the cell surface

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7
Q

PHASE 1 INITIATION: FATE OF IXa

A

 The FIXa does not interact further with the TF-bearing cell and is no longer involved in Phase I: Initiation
 However, if tissue injury has occurred and activated platelets are in the neighborhood, FIXa will diffuse to those platelets, bind to their surface, and (in conjunction with cofactor VIIIa) activate zymogen FX to FXa

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8
Q

phase 1 initiation: Tissue factor in the absence of injury

A

TF-bearing cells appear to bind FVIIa and low levels of FIXa and FXa even in the absence of injury but are separated from the Phase II: Amplification components by the normally intact blood vessel wall.

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9
Q

signal for phase 2 amplification

A

The thrombin generated on the TF- bearing cell serves as the “signal” for Phase II: Amplification to begin

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10
Q

Phase II: Amplification:platelet activation

A

 When sufficient thrombin (FIIa) is generated on or adjacent to TF-bearing cells, platelets are activated
 NOTE: At this point there is not nearly a sufficient amount of thrombin to cause formation of a clot (that is, effectively convert fibrinogen to fibrin)

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11
Q

Phase II: Amplification The small amount of TF-bearing cell- generated thrombin activates:

A

 Activates platelets
 Activates FVa from FV
 Activates FVIIIa and dissociates it from von Willebrand Factor (vWF)
 Activates XIa from XI

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12
Q

first step in phase 3 propagation

A

The production of vast amounts of thrombin on the surface of activated platelets

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13
Q

phase 3 propagation: when vascular injury occurs platelets

A

eave the blood vessel, bind to collagen/vWF/blood vessel wall receptors and other extravascular “stuff”, and are activated by a combination of those factors and the “priming” dose of thrombin
 This adherence of platelets to the damaged tissue is the first step in the formation of the platelet “plug” necessary for primary hemostasis

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14
Q

phase 3 propagation The newly-activated platelets bind

A

FVa and FVIIIa and the FIXa freshly-liberated by the FVIIa/TF complex
 Freshly-generated XIa binds to the freshly-activated platelet (effectively bypassing the need for FXIIa)
 Membrane-bound FXIa keeps on activating FIX to FIXa
 FVIIIa and co-factor FIXa form what is called the “platelet tenase complex (PTC)”

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15
Q

phase 3 propagation The PTC activates even more

A

FX to FXa

 FXa combines with FVa to form the creatively- monikered “Prothrombinase” complex

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16
Q

phase 3:The XaVa “Prothrombinase” complex causes

A

EXPLOSIVE burst of thrombin that helps produce a stable fibrin clot
 Interestingly (well, maybe not to you) it has been discovered that most of the thrombin produced is generated after the initial fibrin clot is formed and that the thrombin produced does other stuff to help the clot such as:
 Continues to activate FXIII and other factors (there are LOTS!)
 Helps to keep constructing the platelet/thrombin clot

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17
Q

Arterial circulation

A

requires rapid response system to seal off any
bleeding sites
 platelets take leading role followed by fibrin formation (antiplatelet agents used to prevent coronary thrombosis)

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18
Q

 Venous circulation

A

 slower response acceptable

 rate of thrombin generation takes leading role (antithrombin agents used to prevent deep venous thrombosis)

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19
Q

What Happens When An Arterial Blood Vessel Is Damaged?

A

 Vascular constriction
 Platelet adhesion
 Platelet activation  formation of the platelet plug
 Activation of cell-based coagulation cascade
 formation of fibrin clot  Clot retraction  Activation of fibrinolytic cascade  Vessel repair / regeneration
Slide 30
Vascular Constriction

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20
Q

Vascular Constriction

A

 Seen when blood vessel itself is injured
 persistent constriction of the smooth muscles
 Most prominent following severe crushing type injuries

21
Q

platelet adhesion problem:

A

Shear stress along vessel wall
 Shear stress inversely related to flow velocity
 Values at vessel wall: 500/sec larger arteries; 5,000/sec arterioles
 Opposes any tendency of flowing blood to clot  limits time available for procoagulant reactions to
occur
 displaces cells or proteins not tightly bound to the vessel wall

22
Q

coaxial migration

A

platelets pushed to vessel perimeter by larger erythrocytes & leukocytes

23
Q

apture” depends on several binding sites such as

A

von Willebrand’s factor (vWf) and collagen

 platelet surface receptor called Glycoprotein Ib (GPIb)

24
Q

vWf held in place by binding to

A

subendothelial collagen

25
Q

GPIb binds easily with vWf, but it is a low-affinity interaction so it

A

slows, but does not stop the platelet – tumbles slowly over endothelium

26
Q

Interaction between platelet GPIb and the vWf molecule causes

A

transmembrane signaling

27
Q

Transmembrane signaling coupled with high shear stress results in

A

activation of platelet

28
Q

platelet activation

A

Platelet loses normal discoid shape  Platelet receptor GPIIb/IIIa undergoes conformational
change
 GPIIb/IIIa now able to bind to another binding site on vWf (GPIIb/IIIa site of action of newer antiplatelet agents)
 high-affinity bond that secures activated platelet to subendothelium
 Subendothelial collagen binds with platelet receptor GPIa/IIa
 at medium shear stress strong enough to bind platelet to subendothelium
 Subendothelial collagen also binds with platelet receptor GPIV which causes activation of the platelet

29
Q

Platelet Activation - Goals

A

Recruitment of additional platelets
 Vasoconstriction of smaller arteries
 Local release of ligands needed for stable platelet-platelet matrix
 Localization and acceleration of platelet-associated fibrin formation
 Protection of clot from fibrinolysis

30
Q

thromboxane

A

A2 (TXA2) important platelet agonist
and vasoconstrictor
 formed in cytosol following cyclooxygenase cleavage of arachidonic acid
 cyclooxygenase activity irreversibly inhibited by aspirin – no TXA2 formation

31
Q

serotonin

A

released from platelet granules - platelet agonist and vasoconstrictor

32
Q

adenosine diphosphate (ADP)

A

released from platelet granules - platelet agonist no known vasoactive role

33
Q

Formation of Platelet Plug

A

Surface receptor GPIIb/IIIa undergoes calcium dependent conformational change
 able to bind with fibrinogen or vWf  Fibrinogen and vWf stored in alpha-granules
within platelet – released following activation
 Fibrinogen and vWf bonds form between platelets binding them together in a tight matrix
 More than 50,000 GPIIb/IIIa receptors present on platelet surface – additional receptor molecules available within cytoplasm

34
Q

clotting factors

A

 I: Fibrinogen  X: Stuart factor; Stuart-
 II: Prothrombin
 III: Tissue thromboplastin
 IV: Calcium
 V: Proaccelerin; Labile factor
 VII: Proconvertin; Stable factor
 VIII: Antihemophilic factor A
 IX: Plasma thromboplastin component; Antihemophilic factor B; Christmas factor
Prower
 XI: Plasma thromboplastin antecedent; Antihemophilic factor C
 XII: Hageman factor; Antihemophilic factor D
 XIII: Fibrin stabilizing factor; Laki-Lorand factor
There is no factor VI

35
Q

Additional Clotting Factors

A

 Prekallikrein
 High-molecular-weight kininogen
 Antithrombin; Antithrombin III
 Lipoprotein-associated coagulation inhibitor (extrinsic pathway inhibitor)
 Antiplasmin  Plasminogen activator inhibitor  alpha2-Macroglobulin  Protein C  Protein S
:

36
Q

Phase IV termination Four autologous anticoagulants help control the spread of coagulation activation:

A

 Tissue Factor Pathway Inhibitor (TFPI)  Protein C (PC)  Protein S (PS)  Antithrombin III (AT or AT-III)

37
Q

TFPI forms a quarternary complex called

A

TF/FVIIa/FXa/TFPI which inactivates various factors and limits coagulation

38
Q

Proteins C and S inactivate

A

FVa and FVIIIa cofactors

39
Q

PC

A

s a vitamin K-dependent plasma glycoprotein which helps break down FVa and FVIIIa
-PC is activated by thrombin (negative feedback loop?) and its activity is increased by PS (which is also vitamin K- dependent)

40
Q

AT

A

inhibits thrombin and the “Serine Proteases” (that might be important later on) such as FIXa, FXa, FXIa, and FXIIa.

41
Q

Fibrinolysis

A

The production of plasmin signals the Fibrinolytic phase of coagulation

42
Q

Plasmin is produced from

A

he zymogen plasminogen by the action of urokinase- type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA)

43
Q

uPA & tPA are regulated by

A

Plasminogen Activator Inhibitors 1 & 2 (PAI-1 & PAI-2)

44
Q

tPA is released by

A

endothelial cells and activated by thrombin (there’s another negative feedback loop) and venous occlusion

45
Q

tPA and plasminogen bind to

A

the growing fibrin polymer as fibrinogen (FI) is converted into fibrin (Fia)

46
Q

plasminogen is activated to plasmin which

A

cleaves fibrin strands

47
Q

fibrinolysis

A

Cleaved fibrin produces Fibrin Degradation Products (FDPs or Fibrin Split Products)
 FDPs are measured to help determine the amount of fibrinolysis occurring (when might that be important?)

48
Q

What effect does coagulation have on cardiac surgery and cardiopulmonary bypass?

A

Bleeding
 bad outcome; increased cost; increased exposure to blood products; increased chance of infection
 Circuit integrity
 large foreign surface stimulates coagulation cascade; concerned with coagulation monitoring / treatment of circuit surface / protocols
 Inflammation  coagulation cascade will stimulate inflammation activities
 Disease state of patient  what patient conditions will affect coagulation status?  diabetes; liver disease; obesity, sepsis

49
Q

Effect of Bypass/Surgery on Coagulation

A

 Activates intrinsic and extrinsic coagulation pathways  large negatively charged surface
 activates intrinsic pathway (which also activates fibrinolysis which activates complement)
 coronary suction  introduces tissue factor from damaged cells which activates
the extrinsic pathway  Activates neutrophils and monocytes
 activation of complement cascade results in leukocyte activation
 Surgery will expose the Subendothelium  stimulates coagulation
 Platelet activation  contact with foreign surface of the circuit  activation of intrinsic and extrinsic pathways
 Vascular endothelial cell activation  not sure how, but it happens

Perf Tech (14 decks)

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