Thrombosis Flashcards
What is the difference between an Anti-coagulant and an clot-buster?
Anti-coagulants prevent blood from clotting whereas clot-busters reverse clotting.
Difference between arterial thrombosis and venous thrombosis?
Arterial thrombosis (platelet rich/white thrombosis) mostly result from atheroma rupture this ends up blocking downstream smaller arteries which stop blood flow and can cause an infarction (MI or stroke) as oxygenated blood cannot reach tissue. Venous thrombosis (platelet poor/red) result from stasis or a hypercoagulant state. If you have a clot blocking flow you will get a back pressure causing oedema. If it dislodges (embolism), it will eventually end up moving into the RV and get stuck in the pulmonary artery or further smaller arteries in the lungs.
What is fibrinolysis?
Getting rid of the clot, it involves an enzyme plasmin cleaving fibrin. Which produces D-dimers (these are just fragments of fibrin which tell you a clot has happened somewhere in the body, important clinical marker).
How do natural endothelial cells in our blood vessels prevent clotting?
Underneath the endothelial cells is tissue factor (initiates clotting) and von Williebrand factor (activates platelets).
The endothelial cells cover this to prevent clotting and release substances such as NO (inhibits platelets), Prostaglandin I2 (PGI-2 inhibits platelets) which are released tonically. The endothelial cells also express Antithrombin on their surface held to the cell by Heparan, antithrombin inhibits many coagulation factors so inhibits clotting. Endothelium also expresses Tissue Plasminogen Activator which activates fibrinolysis (unclots).
What is Virchow’s Triad?
3 things which make a person prone to having a thrombosis, these are:
1) Stasis – static blood lacks kinetic energy and tends to clot
2) Endothelial damage – E.g. due to surgery or cannula
3) Hyper-coagulant state – E.g. infection, heredity, drugs (e.g. HRT) etc.
How can valves in veins lead to a clot forming?
You have turbulence around the valves and it is the turbulence behind the valve that is important, this increases the risk of stasis. Lack of movement in veins causes it to clot. This is the reason people commonly get thrombosis on planes due to lack of movement.
If venous return is blocked due to a thrombus, the affected organ becomes congested with fluid because of the arterial pressure behind, meaning the fluid has nowhere else to go other than out.
What are the 4 potential fates of a thrombus after it has formed?
1) Resolution – Fibrinolytic system destroys the whole clot over time
2) Embolism – Go to heart, go to lungs -> cause death
3) Organised – Endothelial cells just grow over the clot, this makes person more prone to having another one due to a narrower vein.
4) Recanalised and Organised – Thrombus is so big you can’t grow over it but you can grow through it.
What is the difference between a Proximal and Distal DVT?
- Proximal DVT = Higher risk of pulmonary embolism and post-thrombotic syndrome (pain, swelling, possibly ulcers) – as closer to heart and more likely to move to lungs – you should therefore be more worried as it is more dangerous than distal DVT. [External iliac, common femoral, deep femoral]
- Distal DVT (anything below the knee) = Rarely causes a pulmonary embolism and rarely causes post-thrombotic syndrome [Tibial and small saphenous vein] it is more likely to respond to treatment.
What happens when von Willerband factor is expressed?
Von Williebrand factor expressed by subendothelial cells (when endothelial layer has been broken due to damage etc.) activates platelets which bind to the von Willebrand factor. Activated endothelial cells can express von Williebrand factor also.
The activated platelets release Thromboxane A2 and ADP which activate other platelets nearby to get them involved and induce receptors ((called GPIIB/IIIa) GP stands for glycoprotein)) which is a receptor for fibrinogen. Fibrinogen acts as a tether which holds platelets together (note that this isn’t coagulation.
What are some of the substances which can activate platelets?
We have: ADP, Thromboxane A2, Thrombin, Collagen and many more
What happens to the platelets once they have cross linked?
They start to change the charge on their membranes, they turn their phospholipids inside out and this gives a negatively charged surface which is required for successful coagulation.
Draw the clotting cascade.
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