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Secondary fibrinolysis Primary fibrinolysis Plasminogen FDP D-dimer DIC 3P test. Hypercoagulable state Thrombophilia Activated protein C resistance (APCR) Factor V Leiden Antithrombin deficiency Anticoagulant therapy. Week 7: Fibrinolysis and Thrombophilia. Fibrinolysis.

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week 7 fibrinolysis and thrombophilia
Secondary fibrinolysis

Primary fibrinolysis

Plasminogen

FDP

D-dimer

DIC

3P test

Hypercoagulable state

Thrombophilia

Activated protein C resistance (APCR)

Factor V Leiden

Antithrombin deficiency

Anticoagulant therapy

Week 7: Fibrinolysis and Thrombophilia
fibrinolysis
Fibrinolysis
  • Plasminogen Activators
    • Thrombin
    • Tissue plasminogen activator (t-PA)
    • Streptokinase
    • Urokinase
    • Kallikrein
  • Fibrinolysis Inhibitors
    • 2 antiplasmin
    • 2 macroglobulin
fibrin ogen degradation product
Fibrin(ogen) Degradation Product
  • X fragment: D-E-D
  • Y fragment: D-E
  • Smallest fragments: D and E
  • D-dimers from fibrin degradation only (ie, 2o fibrinolysis, not 1o)
fdp screen
FDP Screen
  • Thrombo-Wellco
    • Anti-fibrinogen coated latex
  • D-dimers
    • Positive only with 2o fibrinolysis
  • Plasma protaminesulfate paracoagulation (3P)
    • Dissociate FM-FDP to allow FM to re-associate
    • Also specific to 2o fibrinolysis
disseminated intravascular coagulation
Triggering mechanism

Trauma, injury, surgery

Hemolysis

AML M3

Snake venom

Amniotic fluid

Dead fetus

Gram negative endotoxin

Consumptive

Low PLT

Long PT/APTT

Low fibrinogen

FDP, D-dimer

Schistocyte

Treatment

Remove source of Tpl

Heparin to stop cascade

Disseminated Intravascular Coagulation
slide11
DIC
  • Syndrome, not disease
  • 1:1,000 hospitalized patients, but many asymptomatic
  • Tx: removal of underlying cause if possible
  • Support with FFP, PLT, RBC, etc.
  • Low molecular weight heparin (LMWH)
primary fibrinolysis
Plasminogen activation without clotting

Unknown mechanism

Labs similar to DIC but important differences

PLT unaffected

No schistocyte

Long PT/APTT

Low fibrinogen

FDP but no D-dimer

Primary Fibrinolysis
thrombophilia
Thrombophilia
  • Tendency to form thombi
  • Hereditary and acquired
  • Hypercoagulable state
  • Arterial thrombi: usually in areas of atherosclerotic plaques
  • Venous thrombi: thrombophlebitis, DVT, pulmonary embolism
venous thromboembolism
Venous Thromboembolism
  • Venous stasis
  • Activated protein C resistance, factor V Leiden
  • Protease inhibitor deficiency (antithrombin, protein C, protein S)
hereditary thrombophilia
Antithrombin deficiency

Recurrent DVT

Protein C deficiency

Vitamin K dependent

Inactivated Va and VIIIa

Protein S deficiency

Vitamin K dependent

Protein C cofactor

APCR

Factor V Leiden

Prothrombin gene mutation 20210

Hereditary Thrombophilia
acquired thrombophilia
Acquired Thrombophilia
  • Antiphospholipid antibody: e.g., Lupus-anticoagulant
  • Malignancy
  • Oral contraceptives
  • Post-op and trauma
  • Myeloproliferative disorders
therapies
Heparin

Monitor with APTT

LMWH no HIT

Oral anticoagulants (e.g., Coumadin)

Monitor with PT

Thrombolytic agents (plasminogen activators)

Streptokinase

Urokinase

t-PA

Anti-platelet agents

Aspirin

Plavix

IV inhibitors

Direct thrombin inhibitors (e.g., hirudin - from leech saliva)

Not dependent on AT-III

Act on thrombin’s fibrin binding site

Therapies
problems with oral anticoagulants
Problems with Oral Anticoagulants
  • GI hemorrhage
  • Skin necrosis
  • Antidote: vitamin K
problems with heparin
Problems with Heparin
  • Unfractionated Heparin may cause heparin induced thrombocytopenia (HIT) due to antibody against heparin-PF4 complex
  • LMWH: almost exclusively against Xa, less osteoporosis, less HIT
  • Antidote: protamine sulfate