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Perf tech II > test 6 > Flashcards

test 6 Flashcards

1
Q

Circulatory Homeostasis (hemostasis)

A

 Normal blood circulation is maintained by a system of
checks and balances
 preservation of blood fluidity
 ability to seal off any site of bleeding

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2
Q

Balance of circulatory homeostatis is determined by the number and function of (2)

A

 anticoagulant factors

 procoagulant factors

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3
Q

Arterial circulation and response

A

-high pressure, narrow, flow velocity high
 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)
-use antiplatelet drugs

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4
Q

Venous circulation and response

A

-low pressure, low velocity of flow
 slower response acceptable
 rate of thrombin generation takes leading role (antithrombin agents used to prevent deep venous thrombosis)
-platelets not as important as they are on the arterial side
-use antithrombin agents

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5
Q

anticoagulant factors

A

 released by endothelial cells that line the vascular system (prostacyclin, vascular plasminogen activator)

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6
Q

procoagulant factors

A

 platelets
 plasma proteins – inactive state (zymogen)
 Tend to be activated when the lining of the vascular system is disrupted (endothelial cells damaged or destroyed)
-endothelial lining is not conducive to clot formation
-everything inside and behind the endothelial cells are procoagulants

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7
Q

What Happens When An Arterial Blood Vessel Is Damaged?

A

 Vascular constriction
 Platelet adhesion
 Platelet activation
 formation of the platelet plug (clump and first blockage to prevent leakage)
 Activation of coagulation and formation of fibrin clot**
 Clot retraction
 Activation of fibrinolytic cascade (stops additional coagulation)
 Vessel repair / regeneration

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8
Q

The importance of platelet aggregation and what they do

A

 platelets localize & accelerate process
 provide essential negative phospholipid surface for various reactions
 provide receptor sites for specific cascade factors
 release some of the cascade factors
-not just the number of platelets that is important, but the platelets MUST be activated at the site of the injury

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9
Q

two groups the clotting factors broken down into

A

 Proenzymes (also called zymogens)

 Procofactors

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10
Q

Proenzymes (also called zymogens)

A

 Factors that become enzymes when activated
-then participate in further activity within the clotting process (converting inactivated substances to activated substances)

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11
Q

Procofactors

A
  • once activated they have no enzymatic activty
  • must bind with another active substance (enzyme) to create some type of a complex which enhances the action of the enzyme itself
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12
Q

Additional clotting factors

A

 High-molecular-weight kininogen
 Antithrombin; Antithrombin III
 Antiplasmin
 Plasminogen activator inhibitor

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13
Q

cascade model

A

 Factors are activated in a specific sequence creating

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14
Q

cell-based model

A

 Seems to provide a better representation of what is happening in vitro
 Cascade defined as a series of steps where enzymes and their cofactors cleaved other proenzymes (zymogens) to create the next enzyme in the step
 Some enzymes need to bind with appropriate cofactor to function properly
 Most of the steps were postulated to occur on the surface of phospholipid membranes and required calcium
 Interaction of thrombin with fibrinogen the major exception
 Three pathways (2 entry, 1 common) lead to the production of the fibrin clot

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15
Q

What is the Coagulation Cascade

A

 Series of proteolytic reactions that lead to the formation of a fibrin clot
 Driven by serial activation of various plasma proteins (normally inactive)
 Two points of initiation
-intrinsic and extrinsic
 Common pathway (prothrombin time – PT)

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16
Q

intrinsic initiation

A

 contact activation; exposure to collagen, basement membrane, microfibrillar substance (activated partial thromboplastin time - aPTT)

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17
Q

extrinsic initiation

A

 release of thromboplastin (tissue factor) from damaged tissue (prothrombin time – PT)

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18
Q

What is factor XII activated by and what does it activate?

A

1) Factor XII (Hageman factor) is activated by contact with subendothelial structures. XIIa also interacts with other cascades.
2) Activated XII and cofactor High Molecular Weight Kininogen activate factor XI (Plasma thromboplastin antecedent) making it XIa
- physical contact activates factor XII

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19
Q

FXIIa also activates

A
  • Intrinsic pathway
  • Neutrophils
  • Platelets
  • Fibrinolytic system
  • Compliment cascade
  • Endothelial cells
20
Q

Additional FXIIa activities

A

• Interacts with HMWK to produce bradykinin (vasodilator)
• Interacts with pre kallikrein to form kallikrein
• Potent activator of
neutrophils & fibrinolysis

21
Q

What does factor XIa (Plasma thromboplastin antecedent) do?

A
  • cleave factor IX (Plasma thromboplastin

component) to IXa

22
Q

What does factor IXa (Plasma thromboplastin

component) do?

A
  • in the presence of cofactor phospholipid (has to occur on a cell membrane) and in the presence of activated factor VIII (Antihemophilic factor A)(that whole complex) activates factor X (Stuart factor)
  • thrombin activates factor VIII
23
Q

Extrinsic pathway process

A
  • initiated by the interaction of tissue factor with factor VII (Proconvertin)
  • has to happen on a phospholipid membrane
  • ability to cleave IX to IXa
  • ability to cleave X to Xa
24
Q

Extrinsic pathway

A
  • most common entry way into the cascade
    1) Release of tissue factor (thromboplastin) appears to be the primary entry point into the cascade.
    2) Cells not normally in contact with blood but may be exposed following damage produce tissue factor at rest.
    3) Cells in contact with blood express tissue factor (protein) on membrane surface only after activation.
    4) Tissue factor binds with circulating factor VII
25
Q

prothrombinase complex

A

-Xa in the presence of Va and Ca++ on a phospholipid membrane to convert (factor II) prothrombin into thrombin (factor IIa)

26
Q

What does activated prothrombin (thrombin, factor IIa) interact with and cause?

A
  • interacts with fibrinogen (factor I) cleaving it into fibrin (weak) which begin to bind together and platelets
  • cleaves factor XIII (Fibrin stabilizing factor) to XIIIa which interacts with fibrin strands to slightly change the structure of the fibrin to turn the weak bonds into strong bond of platelets and fibrin
27
Q

what does factor XIIIa do?

A
  • Cross-links fibrin chains & binds alpha2-antiplasmin to fibrin. Protects fibrin from plasminmediated breakdown.
28
Q

high concentration of fibrin, what will happen and what are the threads like

A
  • form a clot

- fibrin threads narrower but a denser aggregation of them which are harder for the fibrinolytic system to break down

29
Q

low concentration of fibrin, what will happen

A
  • still form a clot but the structure of the clot will have a looser mass of fibrin threads and the fibrin threads tend to be bigger
  • easier for fibrinolytic system to break down
30
Q

Pro’s of Cascade Model

A

 Allowed understanding of how the enzymatic steps occur in plasma-based in vitro coagulation
 Allowed understanding of calcium dependence and the development of calcium chelating anticoagulants
 Allowed the development of useful clinical testing and interpretation of the testing results
 Identification of specific factor deficiencies
 Allowed close examination of the properties of the specific enzymes and clearer understanding of associated cofactors

31
Q

Con’s of Cascade Model

A

 Provides a reasonable explanation of how coagulation takes place in plasma or purified protein-based fluid systems where the fluid in NOT moving and there is NO interaction with the endothelial cells of the vascular wall and NO interaction with other cells surfaces
 Does not describe the hemostatic process that is occurring in our bodies (i.e. in vivo)
 States that the extrinsic and intrinsic pathways are able to operate independently in the generation of Xa
 in vivo it has been shown that bleeding will occur if there are factor deficiencies in the extrinsic pathway even of the intrinsic pathway is intact

32
Q

Need for an In Vivo Model

A

 Vascular system is dynamic not static
 Blood comes into contact with many different types of cells
 Some factors may participate in the enzymatic cascade of coagulation in a static situation, but in a dynamic system they appear to have other roles NOT related to hemostasis
 Inflammatory response
 Function of vessel wall
 Cell proliferation
 Needs to be cell bases

33
Q

Cell-Based Model: Thrombin generation occurs during three phases

A

 Initiation phase
 Amplification phase
 Propagation phase

34
Q

Initiation Phase

A

 The activity of the factor VIIa/Tissue Factor complex is the most significant event to initiate coagulation.
-these two are driving forces

35
Q

Initiation Phase (Step 1)

A

-Activation of VII
 Endothelial cell damage (i.e. vascular damage) exposes tissue factor on the surface of the cell
 TF is a receptor and a cofactor for VII / VIIa
 When VII binds TF it is converted to VIIa (don’t know why) and forms VIIa/TF complex (extrinsic tenase complex)

36
Q

Initiation Phase (Step 2): Extrinsic tenase complex (VIIa/TF complex) does what

A

 catalyzes conversion of IX and X to their activated forms (IXa and Xa respectively)
 Within the circulation, IXa is rapidly inhibited by tissue pathway inhibitor (TFPI) and antithrombin (AT)
 If ACTIVATED platelets are close by, IXa will diffuse to those platelets, bind to their surface and in conjunction with cofactor VIIIa activate X to Xa

37
Q

Initiation Phase (Step 3): Xa formed on TF-bearing cell interacts with what and forms

A

 Cofactor Va to form a prothrombinase complex
 Prothrombinase complex generates a small amount of “priming” thrombin on the surface of the TF-bearing cells
 II (Prothrombin) converted to IIa (Thrombin)
 Xa remains on the cell surface
-amount of thrombin isn’t enough to create a clot
-PURPOSE: to recruit platelets

38
Q

Amplification Phase: thrombin generated on the TF-bearing cell serves as

A

 the “signal” for the start of the Amplification Phase
 Amplification Phase sets the stage for large scale thrombin production by activating platelets
 When enough thrombin (IIa) is generated on or near the TF-bearing cells, platelet activation begins
-activation begins when we have enough “priming” thrombin
 At this time there is NOT ENOUGH thrombin present to initiate clot formation
-process taking place in the tissue

39
Q

To generate the amount of thrombin needed to form a clot

A

 the injury must allow the movement of platelets and large proteins to leave the vascular space so they can bind with TF-bearing cells in the extravascular area
 Factors involved in the amplification and propagation phases are larger and cannot pass through an intact vascular membrane

40
Q

Amplification Phase – Step 1: thrombin (IIa) generated during initiation phase
is very busy with

A

 Binds with platelet surface receptors causing platelet activation
 Catalyzes the conversion of V to activated Va
 Catalyzes the splitting of the VIII/vWF (von Willebrand factor) complex
 vWF will mediate platelet adhesion and aggregation
 Thrombin catalyzes conversion of VIII to VIIIa
 Catalyzes the conversion of XI to XIa

41
Q 
Amplification Phase – Step 2: 
Va binds to?
VIIIa binds to?
XIa binds to?
IXa will complex with
A

 Va binds to the activated platelet membrane
 VIIIa binds to the activated platelet membrane
 XIa binds to the activated platelet membrane
 IXa will complex with VIIIa to form the Intrinsic Tenase Complex
 IXa created during initiation phase but not deactivated because activated platelets available

42
Q

Amplification Phase – Platelet Activation: Binding with IIa causes extreme changes to the surface of the platelet

A

 Shape change
 Rearrangement of membrane phospholipids creating procoagulant membrane surface
 Promotes binding of coagulation proteins to activated membrane
 Release of granule contents
 Raw materials for clotting reactions
 Agonists that induce further platelet activation
-these changes are mediated by thrombin activation

43
Q

Propagation Phase

A

 Purpose of propagation phase is to generate huge amounts of thrombin on the surface of the activated platelets
 Remember, platelets are able to leave the blood vessel as a result of vascular injury and are able to bind to underlying collagen, vWF, blood vessel wall, and other extravascular material. This binding (and the “priming” dose of thrombin) start platelet activation
 The adherence of platelets to the damaged tissue is the first step in the formation of the platelet plug which is necessary for primary hemostasis

44
Q

Propagation Phase (Step 1):

A

 Va, VIIIa, and XIa all bind to the surface of the activated platelet
 XIa catalyzes conversion of IX to IXa
 IXa (produced by Extrinsic Tenase Complex AND conversion by XIa on platelet surface) attaches to the bound VIIIa to create the Intrinsic Tenase Complex (also called Platelet Tenase Complex)

45
Q

Propagation Phase (Step 2 & 3)

A

 Intrinsic Tenase Complex begins massive conversion of X to Xa
 Xa binds with Va to form large number of Prothombinase Complexes
 The large number of Prothombinase Complexes creates an explosive conversion of prothrombin (II) to thrombin (IIa) – the “thrombin-burst”

46
Q

Clot formation

A

 The “thrombin-burst” generates enough thrombin so there is a significant amount of fibrinogen converted to fibrin resulting in the formation of the fibrin clot
 Majority of thrombin produced actually produced after the initial fibrin clot has been formed
 Additional thrombin continues to activate XIII and other factors that affect the strength and structure of the fibrin clot

Perf tech II (16 decks)

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