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Pathology- fluid Hemodynamics > hemostasis and coagulation > Flashcards

hemostasis and coagulation Flashcards

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

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?

A

fibrin

25
Q

platelet stabilzation

A
  • 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
Q

summary of platelet aggregation

A
  • 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
Q

how are most coagulation factors found?

A

circulating in an inactivated serine protease

28
Q

coagulation cascade requires

A

complexing with phospholipids and Ca (surface of activated platelets)

29
Q

extrinsic system

A

formation of activated factor VII

  • activation of VII by tissue factor (tissue or endothelial cell injury)
  • probably most important in vivo
30
Q

intrinsic system

A

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
Q

common pathway of pro-thrombin activation

A

X/V/II

  • activation of X by VIIa or IXa
  • activation of II (prothrombin) by Xa and activated Co-factor V
32
Q

what cross-links fibrin

A

factor XIII

33
Q

inhibits of cascade

A

thrombomodulin/factor C
TFPI
anti-thrombotic

34
Q

two different ways to activate factor X

A
  • Factor VIIa

- Factor IXa+VIIIa

35
Q

prothrombin to thrombin

A

Factor Xa in presence of co-factor Va
Xa/Va= IIa (10/5=2)
thrombin (IIa)

36
Q

thrombin

A
  • 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
Q

how does thrombin act on cells?

A

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
Q

local inflammatory cell effects from thrombin

A
  • aggregation of platelets
  • expression of endothelial cell adhesion molecules
  • secretion of NO, PGI2, tPA, and PDGF by endothelial cells
  • activation of neutrophil, monocytes
39
Q

fibrinolytic cascade

A

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
Q

what does plasmin do?

A

degrades fibrin to fibrin degradation products

  • chemotaxis
  • measure of ongoing activation of coagulation system-> DIC
41
Q

natural anti-coagulants: anti-thrombins

A
  • anti-thrombin III inhibits: thrombin, serine proteases (IXa, Xa, XIa, XIIa)
  • activated by binding heparin-like molecules on endothelial cells
42
Q

natural anti-coagulants

A 
anti-thrombin
protein C and S
tissue factor pathway inhibitor 
plasminogen/plasmin system
plasminogen activators
43
Q

protein C and S

A
  • vitamin K dependent
  • inactivate Va and VIIIa (co-factors)
  • mechanism of action of thrombomdulin: protein C inactivation of thrombin, requires protein S
44
Q

tissue factor pathway inhibitor

A
  • secreted by endothelium

- inactivates factor Xa and tissue factor-> VIIa

45
Q

plasminogen/plasmin system

A

plasmin (active form)

  • fibrinolysis
  • inhibits fibrin polymerization
46
Q

plasminogen activators

A

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
Q

therapeutic anti-coagulants

A
  • platelet antagonists
  • coagulation factors
  • fibrinolytic enzymes
48
Q

platelet antagonists

A
  • Aspirin
  • Clopidogrel (Plavix)
  • GpIIb-IIIa blockers
49
Q

aspirin

A

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
Q

Clopidogrel (Plavix)

A

inhibits binding of ADP to low-affinity platelet receptor and subsequent activation (conformational change) to GpIIb/IIIa

51
Q

GpIIb/IIIa blockers

A

-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
Q

coagulation factors

A

heparin
fondaparinux
coumadin, warfain

53
Q

heparin

A

activation of antithrombin III

  • blocks both thrombin and X-activation
  • low molecular weight heparin works better than unfractionaled heparin
54
Q

fondaparinux

A

selective factor X inhibitor

55
Q

coumadin, warfain

A

prevents carboxylation of factors II, VII, IX, X

56
Q

fibrinolytic enzymes

A 
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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