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Hemostasis > Section 7: Regulation and Fibrinolysis > Flashcards

Section 7: Regulation and Fibrinolysis Flashcards

1
Q

Protein C is made where and dependent on what?

A
  • Made in liver
  • Vit K dependent
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2
Q

How is Protein C activated?

A

Thrombin-thrombomodulin complex attached to endothelium can activate Protein C

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3
Q

Protein C functions

A
  • inactivate Va and VIIIa
  • liberates tPA from endothelial cells
  • Protein S is a cofactor
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4
Q

Protein S traits

A
  • Vit K dependent
  • Made in liver
  • Non-proteolytic
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5
Q

Forms of Protein S

A
  • 60% bound to C4b binding protein (complement protein)
  • 40% free (this is the active form in coag)
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6
Q

Protein S function

A

Cofactor to Protein C

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7
Q

Protein Z traits

A
  • Vit K dependent
  • Made in liver
  • Similar structure to other vit K dep factors except no activation site and non-proteolytic
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8
Q

Protein Z functions

A
  • cofactor to Protein Z-Related Protease Inhibitor (ZPI)
  • major role is to degrade Factor Xa
    - need calcium + phospholipids
    - slow-acting on its own
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9
Q

Protein Z-Related Protease Inhibitor (ZPI) traits

A
  • vit K dep
  • made in liver
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10
Q

ZPI functions

A
  • cofactor to Protein Z
  • action accelerated 1000-fold in presence of Protein Z
  • major role is to degrade Factor Xa
  • also degrades Factor XIa on its own
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11
Q

Antithrombin (AT, formerly ATIII) location made and function

A
  • made in liver
  • functions to form irreversible complex with Factors IIa, IXa, Xa, XIa, XIIa, and plasmin to slowly inactivate/neutralize them
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12
Q

Where is heparin found in the body?

A

Mast cells and tissue basophils

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13
Q

Heparin-like substances made by ___

A

Endothelial cells

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14
Q

Heparin cofactor II (HC-II) trait and functions

A
  • made in liver
  • function is specific to IIa neutralization/inactivation
  • HC-II has accelerated activity in presence of heparin but less than AT
  • present in platelets and may play role in thrombin regulation generated on plt surface
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15
Q

Tissue Factor Pathway Inhibitor (TFPI) functions

A
  • low conc extrinsic pathway inhibitor
  • ECs secrete TFPI into plasma
  • TFPI inhibits Tissue Factor/Factor VIIA complex
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16
Q

List endogenous plasminogen activators

A
  • Activated Protein C (APC)
  • Urokinase
  • XIIa and Kallikrein
17
Q

List exogenous plasminogen activators

A
  • tPA
  • streptokinase
  • urokinase
  • recombinant tPA
18
Q

Caveat to using exogenous plasminogen activators

A

They can break down pt’s fibrinogen (bad)

19
Q

What happens to active plasmin that escapes the clot?

A

It gets destroyed by anti-plasmins
conc of plasmin in circulating plasma too low to achieve fibrinogenolysis

20
Q

Plasmin functions

A
  • lyses both fibrin and fibrinogen
  • most plasmin activity occurs within the clot (fibrin major substrate)
  • inactivates Va and VIIIa
  • degrades XIIa into inactive fragments
21
Q

Describe primary fibrinolysis (aka fibrinogenolysis)

A
  1. Plasmin cleaves fibrinogen into X and Y intermediate degradation products (FDP
  2. Plasmin further cleaves fibrinogen into D and E end products
22
Q

Fibrinogen degradation product (FDP) functions

A

FDPs act as coag inhibitors by attaching to fibrin monomer and preventing polymerization and clot formation

23
Q

Describe secondary fibrinolysis (fibrinolysis)

A
  1. Plasmin removes X and Y intermediates too
  2. Plasmin also cleaves fibrin into D and E end products
24
Q

D-dimers

A
  • Fibrin polymers are stabilized by XIIIa, which forms covalent bonds in the D domain to make an insoluble clot
  • Plasmin breaking down fibrin clots results in D-dimers
25
Q

T/F
D-dimers are present in both fibrinolysis and fibrinogenolysis

A

False
D-dimers present only in fibrinolysis

26
Q

alpha2-antiplasmin

A
  • made in liver
  • functions to bind/inactivate free circulating plasmin that broke free from the clot
  • rapid inhibitor that prevents lysis of fibrinogen or degradation of V and VIII
  • not very effective at inactivating plasmin bound to fibrin
27
Q

alpha2-macroglobulin

A
  • not super great at its job but it works if alpha2-antiplasmin gets used up
  • serves as slow plasmin inhibitor and prevents lysis of fibrinogen/degradation of V and VIII
28
Q

Plasminogen Activator Inhibitors (PAI-1 and PAI-2)

A
  • PAI-1 most important inhibitor to plasminogen activator system
  • released from injured ECs and activated platelets
  • function to neutralize/inactivate tPA and urokinase
29
Q

Thrombin Activatable Fibrinolytic Inhibitor (TAFI)

A
  • functions to alter fibrin clot so it’s less recognizable as a substrate for plasmin, thus it inhibits fibrinolysis
  • activated by thrombin/thrombomodulin complex
  • XIa enhances TAFI production
30
Q

Consequences of Factor XIa deficiency in context of TAFI

A

Clot not modified -> increased fibrinolysis -> bleeding

Hemostasis (10 decks)

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