Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Perf Tech > Topic 1 > Flashcards

Topic 1 Flashcards

1
Q

Homeostasis

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Anticoagulant factors are released by

A

Endothelial cells
(prostacyclin, vascular plasminogen activator)
-These tend to be released from the lining of the vascular garden hose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Procoagulant factors include

A

platelets and plasma proteins – inactive state (zymogen)

-These tend to be released when the lining of that vascular garden hose gets disrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Three Phase Model includes

A

Initiation
Amplification
Propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phase I: Initiation- In vivo

A

The activity of the FVIIa/TF (Tissue Factor) complex is THE most significant event to initiate coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phase I: Initiation-

Activation of FVII

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 and forms the FVIIa/TF complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Phase I: Initiation-

After the FVIIa/TF complex activates the FIX and FX zymogens…. then…

A

FXa formed on the TF-bearing cell interacts with cofactor Va to form a prothrombinase complex and generates a very small amount of “priming” thrombin on the surface of TF-bearing cells. FXa remains on the cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phase I: Initiation-

When does FIXa not interact further with the TF-bearing cell and is no longer involved in Phase I: Initiation

A

After the priming thrombin is formed.
However, if tissue injury occurrs and activates near by platelets, FIXa will diffuse to those platelets, bind to their surface, and (in conjunction with cofactor VIIIa) activate zymogen FX to FXa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Phase I: Initiation-

TF-bearing cells appear to bind to

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Whats the signal for Phase II: Amplification

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phase II: Amplification-

When sufficient thrombin (FIIa) is generated on or adjacent to TF-bearing cells…then…

A

platelets are activated

NOTE: At this point there is not nearly a sufficient amount of thrombin to cause formation of a clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
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 vWF
Activates XIa from XI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phase III: Propagation-

First step is…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Phase III: Propagation-

When vascular injury occurs, platelets leave the blood vessel…then…

A

bind to collagen/vWF/blood vessel wall receptors 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Phase III: Propagation-

The newly-activated platelets bind to…

A

FVa and FVIIIa

FIXa is freshly-liberated by the FVIIa/TF complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Phase III: Propagation-

Freshly-generated XIa binds to…

A

the freshly-activated platelet (effectively bypassing the need for FXIIa). Membrane-bound FXIa keeps on activating FIX to FIXa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phase III: Propagation-

FVIIIa and co-factor FIXa form

A

platelet tenase complex (PTC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Phase III: Propagation-

The PTC activates even more…

A

FX to FXa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Phase III: Propagation-

FXa combines with FVa to form

A

Prothrombinase complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Phase III: Propagation-

The XaVa “Prothrombinase” complex causes…

A

the EXPLOSIVE burst of thrombin that helps produce a stable fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Arterial circulation requires

A

rapid response system to seal off any bleeding sites.

-platelets take leading role followed by fibrin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Venous circulation has a

A

slower response.

-rate of thrombin generation takes leading role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Arterial circulation uses what to prevent coronary thrombosis

A

antiplatelet agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Venous circulation uses what to prevent deep venous thrombosis

A

antithrombin agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What Happens When An Arterial Blood Vessel Is Damaged? (7)
1. Vascular constriction 2. Platelet adhesion 3. Platelet activation- formation of the platelet plug 4. Activation of cell-based coagulation cascade- formation of fibrin clot 5. Clot retraction 6. Activation of fibrinolytic cascade 7. Vessel repair / regeneration
26
Vascular Constriction is seen when
blood vessel itself is injured | -persistent constriction of the smooth muscles
27
Vascular Constriction is most prominent following
severe crushing type injuries
28
Describe the smooth muscle layers typically found in blood vessels
1. Tunica Intima -contains the endothelium 2. Tunica Media- circularly arranged smooth muscle cells and sheets of elastin. Maintains blood pressure and continuous blood circulation 3. Tunica Externa- loosely woven collagen fibers protect and reinforce the vessel, and anchor it to surrounding structures
29
Main Platelet Adhesion - PROBLEM
Shear stress along vessel wall
30
Shear stress inversely related to
flow velocity
31
Shear stress values at vessel wall for large arteries
500/sec
32
Shear stress values at vessel wall for arterioles
5,000/sec
33
Shear stress opposes any tendency of flowing blood to clot because it
1. limits time available for procoagulant reactions to occur | 2. displaces cells or proteins not tightly bound to the vessel wall
34
Platelets are able to adhere to cell walls despite shear stress because
platelets are pushed to vessel perimeter by larger erythrocytes & leukocytes (coaxial migration)
35
Platelet Adhesion- | Adhesion must occur very
rapidly – i.e. instantaneously
36
Platelet Adhesion- | “Capture” depends on several binding sites:
- subendothelial molecules of vWf and collagen | - platelet surface receptor: Glycoprotein Ib (GPIb)
37
Platelet Adhesion- | vWf is held in place by binding to
subendothelial collagen
38
Platelet Adhesion- | GPIb binds easily with
vWf, but it is a low-affinity interaction | - - Slows, but does not stop the platelet – tumbles slowly over endothelium
39
Platelet Adhesion- | Interaction between platelet GPIb and the vWf molecule causes
transmembrane signaling
40
Platelet Adhesion- | Transmembrane signaling coupled with high shear stress results in
activation of the platelet
41
After platelet activation, the platelet loses
normal discoid shape
42
Platelet activation- | Platelet receptor GPIIb/IIIa undergoes
conformational change
43
Platelet activation- | GPIIb/IIIa now able to bind to another binding site on...
vWf - high-affinity bond that secures activated platelet to subendothelium - (GPIIb/IIIa site of action of newer antiplatelet agents)
44
Platelet activation- | Subendothelial collagen binds with...
1. platelet receptor GPIa/IIa-at medium shear stress strong enough to bind platelet to subendothelium 2. platelet receptor GPIV which causes activation of the platelet
45
Platelet Activation - Goals (5)
1. Recruitment of additional platelets 2. Vasoconstriction of smaller arteries 3. Local release of ligands needed for stable platelet-platelet matrix 4. Localization and acceleration of platelet-associated fibrin formation 5. Protection of clot from fibrinolysis
46
Activated platelets release
platelet agonists
47
3 platelet agonists
``` Thromboxane A2 (TXA2) Serotonin Adenosine diphosphate (ADP) ```
48
Thromboxane A2 (TXA2)
platelet agonist and vasoconstrictor - formed in cytosol following cyclooxygenase cleavage of arachidonic acid - cyclooxygenase activity irreversibly inhibited by aspirin= no TXA2 formation
49
Serotonin
released from platelet granules - platelet agonist and vasoconstrictor
50
Adenosine diphosphate (ADP)
released from platelet granules - platelet agonist no known vasoactive role
51
Formation of Platelet Plug- | Surface receptor GPIIb/IIIa undergoes
calcium dependent conformational change | -able to bind with fibrinogen or vWf
52
Formation of Platelet Plug- | Fibrinogen and vWf stored in...
alpha-granules within platelet – released following activation
53
Formation of Platelet Plug- | Fibrinogen and vWf bonds form between
platelets binding them together in a tight matrix
54
Formation of Platelet Plug- | More than ______ GPIIb/IIIa receptors present on platelet surface
50,000 | – additional receptor molecules available within cytoplasm
55
Clotting Factor I
Fibrinogen
56
Clotting Factor II
Prothrombin
57
Clotting Factor III
Tissue thromboplastin
58
Clotting Factor IV
Calcium
59
Clotting Factor V
Proaccelerin | Labile factor
60
Clotting Factor VII
Proconvertin | Stable factor
61
Clotting Factor VIII
Antihemophilic factor A
62
Clotting Factor IX
Plasma thromboplastin component Antihemophilic factor B Christmas factor
63
Clotting Factor X
Stuart factor | Stuart-Prower
64
Clotting Factor XI
Plasma thromboplastin antecedent | Antihemophilic factor C
65
Clotting Factor XII
Hageman factor | Antihemophilic factor D
66
Clotting Factor XIII
Fibrin stabilizing factor | Laki-Lorand factor
67
Additional Clotting Factors (9)
1. Prekallikrein 2. High-molecular-weight kininogen 3. Antithrombin; Antithrombin III 4. Lipoprotein-associated coagulation inhibitor (extrinsic pathway inhibitor) 5. Antiplasmin 6. Plasminogen activator inhibitor 7. alpha2-Macroglobulin 8. Protein C 9. Protein S
68
Phase IV: Termination- | 4 autologous anticoagulants help control the spread of coagulation activation
1. Tissue Factor Pathway Inhibitor (TFPI) 2. Protein C (PC) 3. Protein S (PS) 4. Antithrombin III (AT or AT-III)
69
Phase IV: Termination- | TFPI forms a quarternary complex called the
TF/FVIIa/FXa/TFPI which inactivates various factors and limits coagulation
70
Phase IV: Termination- | Proteins C and S inactivate
FVa and FVIIIa cofactors
71
Phase IV: Termination- | PC is a
vitamin K-dependent plasma glycoprotein which helps break down FVa and FVIIIa
72
Phase IV: Termination- | PC is activated by
thrombin (negative feedback loop?) and its activity is increased by PS (which is also vitamin K-dependent)
73
Phase IV: Termination- | AT inhibits thrombin and the
“Serine Proteases”-such as FIXa, FXa, FXIa, and FXIIa
74
Fibrinolysis- | What signals the Fibrinolytic phase of coagulation
The production of plasmin
75
Fibrinolysis- | Plasmin is produced from the zymogen plasminogen by the action of
urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA)
76
Fibrinolysis- | uPA & tPA are regulated by
Plasminogen Activator Inhibitors 1 & 2 (PAI-1 & PAI-2)
77
Fibrinolysis- | tPA is released by
endothelial cells and activated by thrombin (negative feedback loop) and venous occlusion
78
Fibrinolysis- | tPA and plasminogen bind to the
growing fibrin polymer as fibrinogen (FI) is converted into fibrin (Fia)
79
Fibrinolysis- | plasminogen is activated to
plasmin which cleaves fibrin strands
80
Fibrinolysis- | Cleaved fibrin produces
Fibrin Degradation Products (FDPs or Fibrin Split Products)
81
Fibrinolysis- | FDPs are measured to help determine the
amount of fibrinolysis occurring
82
Endogenous Anticoagulants
Prevent clotting – keep blood liquid | Require intact endothelial cell barrier
83
endothelial cells negative charge repels
platelets
84
endothelial release of _______ – inhibit platelet adhesion and aggregation
nitric oxide (endothelium-derived relaxant factor) & prostacyclin (PGI2)
85
endothelial release of ______ – inactivates platelet released ADP limiting ability to recruit other platelets
ADPase
86
Effect of Bypass/Surgery on Coagulation: | Activates what pathways
intrinsic and extrinsic coagulation pathways 1. large negatively charged surface activates intrinsic pathway (which also activates fibrinolysis which activates complement) 2. coronary suction introduces tissue factor from damaged cells which activates the extrinsic pathway
87
Effect of Bypass/Surgery on Coagulation: | Activates what cells
neutrophils and monocytes | -activation of complement cascade results in leukocyte activation
88
Effect of Bypass/Surgery on Coagulation: | Surgery will expose the
Subendothelium | -stimulates coagulation
89
Effect of Bypass/Surgery on Coagulation: | Platelet activation
contact with foreign surface of the circuit | activation of intrinsic and extrinsic pathways
90
Effect of Bypass/Surgery on Coagulation: | _______ cell activation
Vascular endothelial

Perf Tech (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions