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Hypercoagulable States

Inherited hypercoagulable states
  1. Defective inhibition of coagulation factors
    1.  ­ factor V Leiden C (resistant to inhibition by activated protein C)
    2. Protein C deficiency & protein S deficiency
  2. Impair clot lysis (a) dysfibrinogenemia (b) Plasminogen deficiency (c) TPA deficiency (d) ­ PAI - I
  3. Idiopathic
  4. Homocystinuria
    Hypercoagulability due to defective factor V gene.
Factor V Leiden(LQ 2012)
  1. M/C genetic cause of thromboses (LQ 2012)                           
  2. M/C congenital cause of venous thrombosis
  3. M/C hereditary coagulable condition  
Antiphospholipid syndrome (Hypercoagulability)
  1. anti cardiolipin ab                                   
  2. Anti b-2 glycoprotein 1 ab                        
  3. Lupus anticoagulant
  4. Thrombocytopenia                                     
  5. Hemolytic A                                                     
  6. Recurrent abortion
  7. Pregnancy Induce Hypertension             
  8. Thrombotic effects in Artery & Vain           
  9. PTT                 
  10. False +ve VDRL
Other’s causes of False +ve VDRL
1. Recent viral infection                                
2. Immunization                   
3. Genital herpes HIV                         
4. Malaria
5. Parental drugs use                         
6. old Ag                                               
7. Rheumatoid arthritis

Table - Risk Factors for Venous Thrombosis
Acquired Inherited Mixed/Unknown
Major surgery Antithrombin deficiency High levels of factor VIII
Major trauma Protein C deficiency High levels of factor IX
PNH Protein S deficiency High levels of factor XI
Malignancy Factor V Leiden (FVL) High levels of fibrinogen
Antiphospholipid syndrome Prothrombin Hyperhomocysteinemia
Puerperium, Pregnancy Dysfibrinogenemia  
Prolonged bed rest    
Plaster cast    
Hormonal replacement therapy    
Myeloproliferative disorders    
Polycythemia vera    
Long-haul travel    
Old Age    

Site of action of various antiplatelet drug

Fig: The fibrinolytic system and its regulation. Plasminogen activators convert plasminogen to plasmin. Plasmin then degrades fibrin into soluble fibrin degradation products. The system is regulated at two levels. Type 1 plasminogen activator inhibitor (PAI-1) regulates the plasminogen activators, whereas a2-antiplasmin serves as the major inhibitor of plasmin.
The plasminogen – Plasmin System

Examples of fibrinolytic agents:-
  Streptokinase; acylated plasminogen streptokinase activator complex (anistreplase); urokinase; recombinant tissue-type plasminogen activator (rt-PA), which is also known as alteplase or Activase; and two recombinant derivatives of rt-PA, tenecteplase and reteplase.

New Fibrinolytic Agents
Desmoteplase, Alfimeprase, 

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