prevention of thrombophilia
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What are the two primary phases of haemostasis?
- Primary haemostasis: Forms an unstable platelet plug at the site of injury.
2. Secondary haemostasis: Activation of the coagulation cascade to stabilize the plug with fibrin. [Slide 3]
In the "Coagulation Made Easy" model, what are the three pathways involved?
- Intrinsic (measured by PTT)
2. Extrinsic (measured by PT)
3. Common [Slide 5]
What is the mnemonic to remember the clotting factors in the Common Pathway?
The Wallet Mnemonic: Factors in your wallet smaller than £20: 10, 5, 2, and 1 (Factors X, V, II, and I). [Slide 6]
What complex is formed by the combination of Factor Xa, Va, and Calcium?
The prothrombinase complex. [Slide 6]
Which factor corresponds to prothrombin and what is its activated form?
Which factor corresponds to fibrinogen and what is its activated form?
What is the mnemonic to remember the factors in the Intrinsic (PTT) Pathway?
Twelve (XII)
Eleven (XI)
Nine (IX)
Eight (VIII)
Ten (X) [Slides 8-9]
How does the Intrinsic (PTT) pathway compare to the Extrinsic (PT) pathway in terms of response and productivity?
The Intrinsic pathway has a slower response to injury but is quantitatively more productive than the Extrinsic pathway. [Slide 9]
Which clotting factor is unique to the Extrinsic (PT) Pathway?
What specific action is required to remove "fibrinogen caps" to allow fibrin-to-fibrin binding?
The action of Thrombin (Factor IIa). [Slide 11]
Which factor is responsible for stabilizing the fibrin clot by cross-linking fibrin polymers?
What is the primary enzyme responsible for fibrinolysis (degrading the clot)?
What are the breakdown products of a fibrin clot called, and which specific one is a common clinical marker?
What are the clinical indications for Warfarin?
- Prophylaxis of systemic embolism (rheumatic heart disease/AF).
2. Prophylaxis after prosthetic heart valve insertion.
3. Prophylaxis and treatment of DVT and Pulmonary Embolism (PE).
4. Transient Ischaemic Attacks (TIAs). [Slide 16]
What is the Mechanism of Action (MOA) of Warfarin?
It is a Vitamin K antagonist that blocks the reduction of Vitamin K epoxide by inhibiting the enzyme VKOR (Vitamin K Epoxide Reductase). [Slide 17]
Which four clotting factors are Vitamin K-dependent and thus inhibited by Warfarin?
Why must an additional anticoagulant (like Heparin) be provided when starting Warfarin therapy for acute events?
- It takes time for existing Vitamin K-dependent factors to degrade.
2. Warfarin initially inhibits Protein C and S (natural anticoagulants), which can cause a temporary pro-thrombotic state. [Slide 18]
How does Heparin act as an anticoagulant?
It potentiates the action of Antithrombin III, which then inactivates Thrombin (IIa) and Factor Xa. [Slides 19-20]
What are the differences in target factors between Unfractionated Heparin (UFH) and Low Molecular Weight Heparin (LMWH)?
LMWH: More selective for Factor Xa (with less effect on Thrombin/IIa). [Slides 19-20]
Name three examples of Low Molecular Weight Heparins (LMWHs).
- Dalteparin
2. Enoxaparin
3. Tinzaparin [Slide 20]
What is Fondaparinux and what is its specific target?
A synthetic pentasaccharide that selectively inhibits Factor Xa. [Slide 20]
What are the advantages of LMWHs over Unfractionated Heparin?
- More predictable dosing.
2. Less routine monitoring required.
3. Lower risk of Heparin-Induced Thrombocytopenia (HIT). [Slide 21]
What drug is used to reverse the effects of Heparin, and what is its biological source?
What does the acronym NOAC/DOAC stand for?
Which NOAC is a Direct Thrombin (IIa) Inhibitor?
Name three NOACs that are Factor Xa Inhibitors.
- Rivaroxaban
2. Apixaban
3. Edoxaban [Slide 26]
What are the typical indications for DOACs?
- Stroke prevention in non-valvular AF.
2. Treatment/prevention of DVT and PE.
3. Prevention of VTE following hip or knee replacement surgery. [Slide 27]
Compare Warfarin vs. NOACs regarding onset, dosing, and monitoring.
NOACs: Rapid onset, fixed dosing, no routine monitoring required. [Slide 29]
What are the specific reversal agents for Dabigatran and Factor Xa inhibitors?
Apixaban/Rivaroxaban: Andexanet alfa (Ondexxya). [Slide 29]
How does Streptokinase function as a fibrinolytic?
It is an enzyme (secreted by streptococci) that binds to and activates plasminogen to form plasmin. [Slide 31]
What is a major safety concern when reusing Streptokinase?
Because it is a bacterial product, it is targeted by the immune system; there is a risk of allergic reaction/anaphylaxis. It should not be used again after 4 days of the first dose. [Slide 31]
What is Alteplase and what is its Mechanism of Action?
A human recombinant Tissue Plasminogen Activator (tPA); it catalyzes the conversion of plasminogen to plasmin. [Slide 32]
What are the time windows for administering Alteplase in acute MI vs. Ischaemic Stroke?
Ischaemic Stroke: Maximum 4.5 hours from symptom onset. [Slide 32]
What chemicals are released by activated platelets to cause further aggregation?
What is the Mechanism of Action of Aspirin as an antiplatelet?
It irreversibly inhibits Cyclo-oxygenase (COX-1), blocking the production of Thromboxane (A₂). [Slide 35]
How do Clopidogrel, Prasugrel, and Ticagrelor prevent platelet aggregation?
They block the P2Y12 receptor on platelets, inhibiting the binding of ADP. [Slide 35]
What is the Mechanism of Action of Glycoprotein IIb/IIIa inhibitors (e.g., Abciximab, Eptifibatide)?
They block the binding of fibrinogen to the GP IIb/IIIa receptors on the platelet surface, preventing the final common pathway of aggregation. [Slides 35–36]
Should antiplatelets be used for primary prevention of cardiovascular disease?
No, they should not be prescribed routinely for primary prevention; they are mainly used for secondary prevention. [Slide 37]
How do antifibrinolytics (e.g., Tranexamic acid) work?
They inhibit the activation of plasminogen to plasmin, preventing the breakup of fibrin and maintaining clot stability. [Slide 39]
What is the underlying cause of Haemophilia A?
A deficiency in Factor VIII. [Slide 41]
What is the underlying cause of Haemophilia B?
A deficiency in Factor IX (Christmas disease). [Slide 41]
What is the underlying cause of Haemophilia C?
A congenital deficiency in Factor XI. [Slide 41]
What is Von Willebrand Disease?
A deficiency of von Willebrand factor (vWF), which is necessary for platelet adhesion and stabilizes Factor VIII. [Slide 41]
How does Desmopressin (DDAVP) help in mild Haemophilia A or vWD?
It boosts the levels of Factor VIII and vWF. [Slide 42]
What is Octocog alfa?
A recombinant human Factor VIII used for preventative treatment in Haemophilia A. [Slide 43]
What is Nonacog alfa?
A recombinant human Factor IX used for preventative treatment in Haemophilia B. [Slide 43]
Which antiplatelet drugs are typically given IV in secondary care?
What is the clinical marker of successful fibrinolysis?
What is the specific enzyme inhibited by Aspirin?
List three conditions where DOACs are used for prevention of systemic embolism.
- Non-valvular atrial fibrillation (NVAF).
2. Following elective hip replacement.
3. Following elective knee replacement. [Slide 27]