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Perf tech II > test 6 part 2 > Flashcards

test 6 part 2 Flashcards

1
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
         formation of fibrin clot
 Clot retraction
 Activation of fibrinolytic cascade
 Vessel repair / regeneration
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2
Q

Vascular Constriction

A

 Seen when blood vessel itself is injured
 persistent constriction of the smooth muscles (only the smaller vessels)
 Most prominent following severe crushing type
injuries (rather than a slicing wound)
 Constriction requires the presence of smooth
muscle fibers!!

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3
Q

Platelet Adhesion - PROBLEM

A

 Shear stress along vessel wall
 Shear stress inversely related to flow velocity
 Shear stress Values at vessel wall: 500/sec larger arteries; 5,000/sec arterioles (huge amount of shear stress at the wall of each vessel)
 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
 GOOD NEWS: platelets pushed to vessel perimeter by larger erythrocytes & leukocytes (coaxial migration)

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4
Q

Platelet Adhesion – vWf, GPIb Interaction

A

 Adhesion must occur very rapidly – i.e. instantaneously
 “Capture” depends on several binding sites
 subendothelial molecules of von Willebrand’s factor (vWf) and collagen
 platelet surface receptor called Glycoprotein Ib (GPIb)
 vWf held in place by binding to subendothelial collagen
 GPIb binds easily with vWf, but it is a low-affinity interaction - - Slows, but does not stop the platelet —tumbles slowly over endothelium
-two steps: 1. slows them down.
-2. forms stronger bond
to stop the platelet in place
-high attraction with low affinity
 Interaction between platelet GPIb and the vWf molecule causes transmembrane signaling
 Transmembrane signaling coupled with high shear stress results in activation of the platelet

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5
Q

Platelet Activation

A

 Platelet loses normal discoid shape
 Platelet receptor GPIIb/IIIa undergoes conformational change and becomes active and is now able to bind to the vWf
 GPIIb/IIIa (glycoprotein) 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

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6
Q

Simplified version of platelet activation

A

1) GPIb binds with vWf = initial activation
2) GPIIb/IIIa binds with vWf = holder
3) GPIa/IIa binds with subendothelial collagen = holder
4) GPIV binds with collagen = continues enhancing activation process (additional transmembrane signaling)

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7
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

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8
Q

Recruitment of Additional Platelets: activated platelets agonists (3)

A

 Thromboxane 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 (platelets don’t get produced)
 Serotonin released from platelet granules - platelet agonist and vasoconstrictor
 Adenosine diphosphate (ADP) released from platelet granules - platelet agonist no known vasoactive role

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9
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 (ensures very good binding between the platelets => very strong platelet plug)

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10
Q

Termination Phase of Clot Formation

A

 Even as the fibrin clot is forming, the Termination system (Fibrinolysis) is being initiated
 Fibrinolysis will disrupt the clotting process and the clot itself

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11
Q

Four naturally occurring anticoagulants help control the spread of coagulation activation

A

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

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12
Q

Tissue Factor Pathway Inhibitor

A

-Forms a four part complex:
 TF/VIIa/Xa/TFPI
-Result:
 Inactivates the factors and inhibits formation of the “priming” dose of thrombin which inhibits coagulation process

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13
Q

Protein C & Protein S

A

 Both inactivate Va and VIIIa

  • can’t convert prothrombin to thrombin
  • concentration driven
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14
Q

Protein C

A

 It is a vitamin K-dependent plasma glycoprotein
-formed by the liver
 Helps break down Va VIIIa
 It is activated by thrombin
 Negative feedback loop??
-as [thrombin] goes up, an [anticoagulant] (protein C) goes up
 Overall activity increased by Protein S
 Protein S is also vitamin K-dependent

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15
Q

Antithrombin III

A 
 Inhibits the action of thrombin
 Inhibits action of other serine proteases
         IXa
         Xa
         XIa
         XIIa
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16
Q

Fibrinolysis

A

 The production of plasmin signals the fibrinolytic phase of coagulation

17
Q

Plasmin is produced from

A
  • plasminogen (zymogen)
18
Q

Plasmin is produced from
plasminogen (zymogen) by
the action of

A

 Urokinase-type plasminogen activator (uPA)
 Tissue -type plasminogen activator (tPA)
 Released by endothelial cells
 Activated by thrombin (negative feedback??) and venous occlusion
-Factor XIa, XIIa, and Kallikrein

19
Q

Action of Fibrinolysis

A

 tPA and plasminogen bind to growing fibrin polymer as fibrinogen (I) is converted to
fibrin (Ia)
 Plasminogen is activated to plasmin which cleaved fibrin strands
 Cleaved fibrin produces Fibrin Degradation Products (FDPs or Fibrin Split Products)
 FDPs are measured to help determine amount of fibrinolysis that is occuring

20
Q

Endogenous Anticoagulants

A

 Prevent clotting – keep blood liquid
 Require intact endothelial cell barrier (minimize tissue factor bearing receptors)
 Arterial vessels
 velocity of blood flow
 endothelial cells negative charge repels platelets
 endothelial release of nitric oxide (endothelium-derived relaxant factor) & prostacyclin (PGI2 ) – inhibit platelet adhesion and aggregation
 endothelial release of ADPase – inactivates platelet released ADP limiting ability to recruit other platelets

21
Q

Anytime you activate something, what happens

A
  • everything else becomes activated
22
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

23
Q

Effect of Bypass/Surgery on Coagulation

A

 Activates intrinsic and extrinsic coagulation pathways
 large negatively charged surface: activates intrinsic pathway
 coronary suction: activates extrinsic pathway by introducing tissue factor from damaged cells
 Activates neutrophils and monocytes
 Surgery will expose the Subendothelium = coagulation stimulation
 Platelet activation
 Vascular endothelial cell activation

24
Q

mechanical bleeding causes

A
  • surgical leak
25
Q

Insufficient fibrin formation

A
  • thrombin inhibition
  • insufficient fibrinogen
  • insufficient thrombin generation
26
Q

insufficient clot integrity

A
  • insufficient fibrin formation
  • insufficient fibrinogen
  • insufficient thrombin generation
  • platelet dysfunction
  • insufficient platelet number
27
Q

insufficient clot adhesion

A
  • insufficient GPIb function

- insufficient vWf

28
Q

fibrinolysis

A
  • Primary: pathological plasmin

- secondary: physiological plasmin

Perf tech II (16 decks)

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