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Pray to the Hemostatic Deities for Mercy (Exam II) > Regulation Mechanics > Flashcards

Regulation Mechanics Flashcards

Pray to the Hemostatic Deities for Mercy

1
Q

List of Procoagulants

A
  • Coag Factors
  • Collagen/Vasculature
  • Platelets
  • vWF
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2
Q

List of Anticoagulants

A
  • Protein Z & ZPI
  • TFPI
  • Antithrombin
  • Heparin Cofactor II
  • Protein C & Protein S
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3
Q

List of Profibrinolytics

A
  • Plasminogen → Plasmin
  • Kallikrein & XIIa
  • Urokinase
  • Protein C & Protein S
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4
Q

List of Antifibrinolytics

A
  • Antithrombin
  • α2-antiplasmin
  • α2-macroglobulin
  • TAFI
  • PAI 1 (most common) & 2 (lesser)
  • Factor XIa
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5
Q

Anticoagulant Function

Warfarin

Not Naturally in Body

A

Inhibits the Vit K dependent Magic Four (II, VII, IX, X)

Keeps Vitamin K in storage form and unable to be properly utilized

Also technically inhibits anticoagulants that are Vit K dependent

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6
Q

Anticoagulant Function

Protein Z

A
  • Vitamin K dependent
  • Produced in Liver
  • Cofactor to ZPI
  • Major role is degrading Xa
  • Slow acting on it’s own
  • Requires Ca2+ and Phospholipids

Non-proteolytic & no activation site, unlike Vit K dependent factors

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7
Q

Anticoagulant Function

Protein Z-Related Protease Inhibitor (ZPI)

A
  • Vitamin K dependent
  • Produced in Liver
  • Cofactor to Protein Z
  • Accelerated 1000x by Protein Z
  • Major role of degrading Factor Xa
  • Minor role of degrading Factor XIa (does not require Protein Z for this aspect)
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8
Q

Anticoagulant Function

Tissue Factor Pathway Inhibitor (TFPI)

A
  • Low Concentration Inhibitor of Extrinsic Pathway
  • Secreted into plasma by Endothelial Cells
  • Inhibits TF3/VIIa complex (Extrinsic Tenase Complex)
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9
Q

Anticoagulant Function

Antithrombin (AT)

A
  • Produced in Liver
  • Forms irreversible complex w/ Factors IIa, IXa, Xa, XIa, XIIa, and plasmin; leading to slow neutralization
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10
Q

Anticoagulant Function

Antithrombin Interaction with Heparin

A
  • Heparin causes conformational change in AT that increases inhibitory effect
  • Heparin is not consumed in this process, can dissociate and serve as cofactor for additional AT molecules
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11
Q

Anticoagulant Function

Heparin Therapy Effects on AT Levels

A
  • Often results in decreased levels of circulating AT
  • Enhanced AT can lead has a negative feedback loop with itself
  • Can predispose a patient to thrombosis if not weaned off Heparin properly while oral anticoagulants are being introduced
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12
Q

Anticoagulant Function

Heparin Cofactor II (HC-II)

A
  • Produced by Liver
  • Specificity solely to Thrombin (IIa) neutralization
  • Accelerated activity in presence of Heparin (but less than boosted AT)
  • Also present in platelets and may play a role in platelet surface thrombin regulation

Think HC-II in relation to IIa neutralization

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13
Q

Anticoagulant Function

Protein C

A
  • Vitamin K dependent
  • Produced in the Liver
  • Activation via Thrombin-Thrombolmodulin complex
  • Inactivates Va and VIIIa
  • Liberates tPA from Endothelial Cells
  • Protein S is cofactor
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14
Q

Anticoagulant Function

Protein S

A
  • Vitamin K dependent
  • Produced in Liver
  • Non-proteolytic
  • 60% bound to C4b
  • 40% free - this is the active anticoag molecule
  • Serves as Cofactor for Protein C
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15
Q

Anticoagulant Function

Inhibited by Activated Protein C

A

Factors Va & VIIIa

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16
Q

Profibrinolytic Function

Plasmin

A
  • Lyses Fibrinogen (1° Fibrinolysis) & Fibrin (2° Fibrinolysis) - Major Function
  • Inactivates Va & VIIIa
  • Degrades XIIa into inactive fragments
17
Q

Profibrinolytic Function

Activated Protein C

A

Liberates Tissue Plasminogen Activator (tPA) from Endothelial Cells

18
Q

Profibrinolytic Function

Plasminogen Activators

Endogenous

A
  • Urokinase
  • Kallikrein & XIIa
  • Activated Protein C → Liberated tPA

Some evidence that XIa plays a minor role

19
Q

Profibrinolytic Function

Plasminogen Activators

Exogenous

A
  • tPA
  • Streptokinase
  • Urokinase
20
Q

Antifibrinolytic Function

Antithrombin

A

Plasmin bound in irreversible complex that forms along with IIa, IXa, Xa, XIa, XIIa

21
Q

Antifibrinolytic Function

α2-Antiplasmin

A
  • Produced in Liver
  • Binds & Inactivates free circulating plasmin
  • Rapid inhibitor
  • Prevents lysis of of fibrinogen
  • Prevents degradation of Factors V & VIII

Not very effective at inactivating plasmin already bound to fibrin

22
Q

Antifibrinolytic Function

α2-Macroglobulin

A
  • Serves as plasmin inhibitor ONLY when α2-Antiplasmin binding sites are saturated
  • Slower inhibitor than α2-Antiplasmin
  • Same functions as α2-Antiplasmin
23
Q

Antifibrinolytic Function

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

A
  • Most important inhibitor to the plasminogen activator system is PAI-1
  • Released from injured endothelial cells and activated platelets
  • Functions to neutralize tPA (and urokinase)
24
Q

Antifibrinolytic Function

Thrombin Activatable Fibrinolytic Inhibitor (TAFI)

A
  • Activated by Thrombin-Thrombomodulin complex
  • Functions to alter the fibrin clot to make it less recognizable by plasmin, therefore inhibiting fibrinolysis
  • Enhanced by Factor XIa
25
Q

Antifibrinolytic Function

Factor XIa

A

Enhances TAFI production

Deficit leads to unmodified clots and increased fibrinolysis & bleeding

26
Q

Results of Deficiencies

Anticoagulants

A

Thrombosis

27
Q

Results of Deficiencies

Profibrinolytics

A

Thrombosis

28
Q

Results of Deficiencies

Antifibrinolytics

A

Bleeding Issues

29
Q

Results of Deficiencies

Procoagulants (Non-Exceptions)

A

Bleeding Issues

30
Q

Results of Deficiencies

Procoagulants (XIIa)

A

Thrombosis

31
Q

Results of Deficiencies

Procoagulants (PK)

A

Thrombosis

32
Q

Results of Deficiencies

Procoagulants (HWMK)

A

Thrombosis

33
Q

Results of Deficiencies

Procoagulants (Factor I/Ia Dysfunction)

A

Unable to be recognized by Plasmin → Can’t be broken down → Thrombosis

Pray to the Hemostatic Deities for Mercy (Exam II) (2 decks)

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