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Pathology- fluid Hemodynamics > hemostasis and coagulation > Flashcards

hemostasis and coagulation Flashcards

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1
Q

endothelial cells

A

reversal of anti-thrombic properties

  • anti-platelet effects
  • anti-coagulant effect
  • Fibrinolytic effect
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2
Q

platelets

A

formation of primary, secondary platelet plugs

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3
Q

coagulation cascade purpose

A

formation of fibrin

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4
Q

in resting state, intact endothelium….

A

inhibit binding and coagulation factor activation

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5
Q

anti-thrombic properties of endothelial cells

A

anti-coagulation effects
-membrane associated heparin-like molecules-> interact with anti-thrombin III to inactivate thrombin
thrombomodulin
tissue factor pathway inhibitor

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6
Q

thrombomodulin

A

binds thrombin to activated protein C

  • inactivates Va and VIIIa
  • requires protein S
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7
Q

antiplatelet effects of endothelial cells

A
  • coverage of underlying ECM
  • production of vasodilators: prostacyclin, NO
  • adenosine disphosphate: degrades ADP
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8
Q

fibrinolytic effect of endothelial cells

A

synthesizes tissue-type plasminogen activator

-promotes fibrinolysis

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9
Q

what initiates blood coagulation?

A
  • exposure of ECM (collagen)
  • release of tissue factor
  • activation of endothelium by bacterial products and cytokines
  • stasis
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10
Q

platelet plus formation results from

A

activation of platelets and overcoming the anti-thrombotic effect of the endothelium

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11
Q

pro-thrombotic properties of endothelial cells

A
  • production of vWF-> binding of platelets to ECM
  • formation of tissue factor: bacterial endotoxin, cytokine (IL-1, TNF)
  • secretion of plasminogen activator inhibitors
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12
Q

what promotes platelet aggregation and coagulation?

A

endothelial injury or activation

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13
Q

formation of platelet plug

A
  1. platelet adhesion
  2. platelet activation and secretion
  3. platelet aggregation
  4. platelet plug stabilization by fibrin
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14
Q

platelet adhesion

A
  • binding to exposed collagen (ECM and basement membrane) by vWF bridging
  • vWF
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15
Q

vWF

A

synthesized by endothelial cells (stored in Weilbel-Palade bodies)
-bridge binding collagen to platelet via gp1b receptor

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16
Q

Bernard-Soulier Syndrome

A

defects vWF or gp1b result in decreased platelet adhesion

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17
Q

platelet activation and secretion

A
  1. Similar to other inflammatory cells: requires Ca, synthesis of thromboxane from a.a. release
  2. Alpha granules
    - express P-selectin on their membrane
    - contain fibrinogen, fibronectin, factors V and VIII, platelet factor 4 (a heparin-binding chemokine), beta-thrombomglobulin, PGDF, and TGF-beta
  3. Dense bodies
    - ADP, ATP
    - ionized calcium
    - histamine, serotonin
    - epinephrine
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18
Q

activation of dense bodies causes

A

leads to expression of phospholipid complexes required for clotting factor assembly

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19
Q

stimulators of platelet aggregation

A

ADP
TxA2
Thrombin

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20
Q

ADP

A

highly potent mediator of platelet aggregation

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21
Q

TxA2

A
  • production by platelets

- also causes vasoconstriction

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22
Q

thrombin

A
  • formed by activation of coagulation cascade

- binds to thrombin receptors on platelets

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23
Q

platelet aggregration

Study These Flashcards
A
  • autocatylitic release of ADP and thromboxane A2 to build a platelet aggregate
  • platelets bind to each other through bidirectional binding of fibrinogen to GpIIb-IIIa
  • initial aggregation forms primary hemostatic plug (reversible)
  • FURTHER activation results from contraction platelets to from secondary hemostatic plug (irreversible)
24
Q

what stabilizes platelet plug?

25
platelet stabilzation
- fibrin binds to gp IIb/IIIa - cleavage of fibrinogen by thrombin (end result of coagulation cascade) - entrapment of RBC's and leukocytes that contribute to local inflammatory reaction - generation of fibrin split products by the action of plasmin results in further chemotaxis of neutrophils
26
summary of platelet aggregation
- platelets adhere at sites of endothelial injury and become activated - activated platelets secrete granule contents (ADP, fibrinogen, Ca) and synthesize thromboxane - after formation of primary hemostatic plug, platelets contract to form secondary hemostatic plug (aggregation) - stabilization and anchoring of platelet plug by formation of fibrin
27
how are most coagulation factors found?
circulating in an inactivated serine protease
28
coagulation cascade requires
complexing with phospholipids and Ca (surface of activated platelets)
29
extrinsic system
formation of activated factor VII - activation of VII by tissue factor (tissue or endothelial cell injury) - probably most important in vivo
30
intrinsic system
formation of activated factor IX - activation of Hageman factor XIII - sequential activation of XI and IX - activation of factor X by IXa requires factor VIIIa as a co-factor - hereditary absence of VIII or IX results in hemophilia - factor IX can also be activated by VIIa
31
common pathway of pro-thrombin activation
X/V/II - activation of X by VIIa or IXa - activation of II (prothrombin) by Xa and activated Co-factor V
32
what cross-links fibrin
factor XIII
33
inhibits of cascade
thrombomodulin/factor C TFPI anti-thrombotic
34
two different ways to activate factor X
- Factor VIIa | - Factor IXa+VIIIa
35
prothrombin to thrombin
Factor Xa in presence of co-factor Va Xa/Va= IIa (10/5=2) thrombin (IIa)
36
thrombin
- Cleaves fibrinogen to form fibrin - Activates co-factors VIII and V - Activates factor XIII that cross-links fibrin - Binds to thrombomodulin to activate protein C-> thus inhibiting further thrombin synthesis
37
how does thrombin act on cells?
via protease-activated receptors (PAR's) that are linked to G protein (7-spanning receptor family) - clips the ends of the receptors to result in conformation change of the receptor - induced local inflammatory cell effects
38
local inflammatory cell effects from thrombin
- aggregation of platelets - expression of endothelial cell adhesion molecules - secretion of NO, PGI2, tPA, and PDGF by endothelial cells - activation of neutrophil, monocytes
39
fibrinolytic cascade
activation of plasminogen by plasminogen activator to form plasmin - PAI-1 inhibits this process - plasmin degradation of fibrin - allows for eventual dissolution of clot
40
what does plasmin do?
degrades fibrin to fibrin degradation products - chemotaxis - measure of ongoing activation of coagulation system-> DIC
41
natural anti-coagulants: anti-thrombins
- anti-thrombin III inhibits: thrombin, serine proteases (IXa, Xa, XIa, XIIa) - activated by binding heparin-like molecules on endothelial cells
42
natural anti-coagulants
``` anti-thrombin protein C and S tissue factor pathway inhibitor plasminogen/plasmin system plasminogen activators ```
43
protein C and S
- vitamin K dependent - inactivate Va and VIIIa (co-factors) - mechanism of action of thrombomdulin: protein C inactivation of thrombin, requires protein S
44
tissue factor pathway inhibitor
- secreted by endothelium | - inactivates factor Xa and tissue factor-> VIIa
45
plasminogen/plasmin system
plasmin (active form) - fibrinolysis - inhibits fibrin polymerization
46
plasminogen activators
plasminogen-> plasmin - urokinase-like plasminogen activators (u-PA): activates plasminogen in fluid phase - tissue-type plasminogen activators (t-PA): produced by endothelium, activated when bound to fibrin
47
therapeutic anti-coagulants
- platelet antagonists - coagulation factors - fibrinolytic enzymes
48
platelet antagonists
- Aspirin - Clopidogrel (Plavix) - GpIIb-IIIa blockers
49
aspirin
inhibition of cyclo-oxygenase and thromboxane synthesis - irreversible inactivation of platelets: requires several days to replace platelets - effective only in low dose: high dose inhibits prostacyclin
50
Clopidogrel (Plavix)
inhibits binding of ADP to low-affinity platelet receptor and subsequent activation (conformational change) to GpIIb/IIIa
51
GpIIb/IIIa blockers
-platelet integrin that binds fibrinogen to link platelets together -used to prevent secondary thrombosis -individual agents: Eptifibatide (integrilin)-GpIIb/IIa antagonist Tirofiban (aggrastat)-GpIIb/III antagonist Abciximab (ReoPro)-mAb that binds to GpIIb/IIIa receptor
52
coagulation factors
heparin fondaparinux coumadin, warfain
53
heparin
activation of antithrombin III - blocks both thrombin and X-activation - low molecular weight heparin works better than unfractionaled heparin
54
fondaparinux
selective factor X inhibitor
55
coumadin, warfain
prevents carboxylation of factors II, VII, IX, X
56
fibrinolytic enzymes
``` streptokinase urokinase t-PA third generation agents -Alteplase (activase) -Reteplase (rPA, retavase): Activates fibrin-bound plasminogen -Tenecteplase (TNK-t-PA, TNKase): more resistant to PAI-1 -Lanoteplase (n-PA) (novel PA) ```

Pathology- fluid Hemodynamics (4 decks)

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