Untitled Deck Flashcards
What are coagulation disorders?
Conditions affecting the blood’s ability to clot, leading to excessive bleeding or thrombosis.
What activates the intrinsic pathway?
Activated by damage inside the blood vessel.
Factors involved: I, II, IX, X, XI, XII
I = fibrinogen
II = prothrombin
XII = Hagemman factor.
What triggers the extrinsic pathway?
Triggered by external trauma.
I, II, VII, X
Factor VII and tissue factor (TF) are key.
What is the common pathway in coagulation?
Both pathways converge to activate factor X, leading to thrombin formation and fibrin clot development.
What are the types of coagulation disorders?
Can be inherited (e.g., haemophilia) or acquired (e.g., DIC).
What is an example of an antifibrinolytic agent?
Tranexamic acid.
What is used for warfarin reversal?
Vitamin K and Octaplex.
What are recombinant clotting factors?
Safer and virus-free products (e.g., Eloctate for factor VIII).
What are plasma-derived products?
Viral inactivated products, including cryoprecipitate (contains fibrinogen, vWF, and factor VIII).
What are monoclonal antibody columns used for?
Used for purification of clotting factors.
How is Haemophilia A diagnosed?
Prolonged activated partial thromboplastin time (aPTT).
Factor VIII levels <1% indicate severe disease.
What is the therapy for Haemophilia A?
Recombinant factor VIII.
Desmopressin (DDAVP) for mild cases; Tranexamic acid for mucosal bleeds.
What percentage of Haemophilia A patients develop inhibitors?
15% of patients develop inhibitors (antibodies against factor VIII).
How are inhibitors in Haemophilia A managed?
Managed by high-dose factor VIII or bypassing agents (e.g., FEIBA, factor VIIa).
What is the evolution of factor concentrates?
Transitioned from plasma-derived products to recombinant factors.
Current products, like Eloctate, are recombinant and safer.
What causes Haemophilia B?
Caused by factor IX deficiency.
How is Haemophilia B managed?
Managed with recombinant factor IX or plasma-derived products.
What are the types of Von Willebrand Disease (vWD)?
Type 1: Reduced vWF levels (most common); Type 2: Defective vWF function; Type 3: Severe deficiency of vWF.
What is the treatment for Type 1 vWD?
Desmopressin or tranexamic acid.
What is the treatment for Type 2 vWD?
vWF concentrates (e.g., Willate).
What is the treatment for Type 3 vWD?
vWF concentrates; DDAVP is ineffective.
What is DIC?
Acquired thrombophilia characterized by widespread clotting and subsequent bleeding due to depletion of clotting factors.
What are common triggers for DIC?
Sepsis, trauma, malignancy.
How is DIC managed?
By treating the underlying cause and supportive care (e.g., plasma, platelets).
What constitutes a massive transfusion?
Replacement of >50% blood volume within 24 hours.
What are the risks of massive transfusion?
Dilutional coagulopathy, hypocalcemia, and hypothermia.
What is thrombophilia?
Hypercoagulable states that increase thrombosis risk.
What are the causes of thrombophilia?
Can be inherited (e.g., Factor V Leiden) or acquired (e.g., antiphospholipid syndrome).
How is thrombophilia managed?
With anticoagulants and lifestyle modifications.
What does tranexamic acid do?
Prevents clot breakdown by inhibiting plasminogen activation.
What are historical challenges of transfusion-transmitted infections?
Included HIV and hepatitis C transmission.
What are current safeguards against transfusion-transmitted infections?
Viral inactivation methods and nucleic acid testing (NAT).
How is warfarin reversal managed in mild cases?
Skip a dose or administer vitamin K.
What is the preferred treatment for severe warfarin reversal?
Octaplex preferred over plasma to reduce complications.
What are the methods for pathogen inactivation of products?
Solvent detergent treatment, heat inactivation, and pasteurization.
What are examples of resistant pathogens?
Hepatitis B and parvovirus B19.
