Haemostasis and Coagulation Concepts

Haemostasis/Coagulation

• Coagulation is a complex system involving vessels, platelets, and factors. The process of clot formation and removal depends on many interacting forces.
• Haemostasis relies on a balance between thrombosis (blood clot formation) and haemorrhage (bleeding). Procoagulants and anticoagulants need to be in balance.
• Thrombosis is the activation of the haemostatic system at an inappropriate time or location in a blood vessel. Pathological thrombi occur outside the normal haemostatic process.
• Decreased physiological anticoagulants lead to clot formation.
• Decreased procoagulants or clotting factors lead to bleeding. Haemorrhage can stem from vessel disease, rupture, or abnormalities (acquired/congenital).
• Haemostasis involves the vascular system, platelets, and coagulation factors. It aims to stop bleeding from a vessel defect while maintaining blood fluidity.
• Coagulation is split into primary and secondary systems.
  • Primary haemostasis involves platelet function and vasoconstriction.
  • Secondary haemostasis involves coagulation proteins and enzymatic reactions.
  • During secondary haemostasis, fibrin is formed to reinforce the platelet plug until healing occurs.
  • The coagulation cascade results in the conversion of soluble fibrinogen to insoluble fibrin, forming the clot.
  • Thrombin, produced from prothrombin, is crucial in this process.
• The vascular system prevents bleeding through vessel contraction, diverting blood flow away from damaged vessels. Blood vessel walls comprise fibrous tissue like collagen and elastin, and smooth muscle.
• Arteries carry oxygenated blood away from the heart, veins return blood to the heart, and capillaries are tiny blood vessels facilitating material exchange.
• The process of vasoconstriction begins with injury. The initial response is vasoconstriction in arterioles to reduce blood flow to the wound. The blood vessel lining, endothelium, is usually exposed, however, deeper layers can be exposed and become targets.
• Vasoconstriction is caused by molecules like serotonin and thromboxane A2 interacting with receptors on blood vessel cells.
• Endothelial cells control vascular functions, negatively charged to repel blood proteins/platelets under normal conditions. Vasoconstriction is effective in small vessels but needs additional systems for larger vessels.
• The endothelium contains collagen and elastin to regulate permeability and stimulate thrombosis following damage. Platelets bind to the subendothelial connective tissues.
• Von Willebrand factor (vWF) and fibrinogen are crucial in platelet plug formation and clot formation.
• Receptor molecules help platelets bind to damaged vessels and collagen.
• Vessel injury initiates platelet stimulation/activation and platelet shape changes from round to spiny, releasing proteins to attract more platelets.
• Collagen and thrombin promote platelet aggregation, forming a mesh to plug the injury.
• Platelet activation releases proteins (like ADP, thromboxane A2, serotonin) to aid aggregation and promote various reactions.
• Platelets form a template on a lipoprotein surface activating tissue factor. A balance between coagulation proteins and anticoagulants shifts towards coagulation.
• Primary hemostasis has three stages: vasoconstriction, platelet adhesion, and platelet aggregation, leading to a platelet plug.
• Secondary hemostasis involves the coagulation cascade and fibrin formation, culminating in the blood clot.
• Tertiary hemostasis includes fibrinolysis, dissolving the clot after healing.

Platelet System

• Platelets are tiny blood cells involved in clotting to stop bleeding. Damage to blood vessels sends signals to platelets.
• Platelets adhere to the injury site, growing sticky tentacles and attracting more platelets (adhesion). The more platelets pile on top (aggregation), forming a plug to fix the damage.
• Platelets are created from megakaryocytes in the bone marrow. They survive for 8-10 days in the bloodstream. Platelets are non-nucleated, disc-shaped cells. They have unique features like plasma membrane, cytoskeleton and others.
• The structure of platelets relates to their action in blood clotting and platelet aggregation.
• Platelets have specialized receptors, including GPVI, GPIb/V/IX, allbβ3, α2β1, PAR1, PAR4. They also contain substances like ADP, TXA2, and serotonin.
• The sequential development of platelets comes from a hemocytoblast to a megakaryoblast to a promegakaryocyte, and to a megakaryocyte and then to platelets.
• Megakaryocytes are giant cells with multiple copies of DNA, breaking off to form platelets.

Vascular System

• The vascular system, also known as the circulatory system, comprises the network of blood and lymph vessels.
• Arteries and veins transport blood, delivering nutrients and oxygen, and carrying away waste matter. Capillaries connect arteries and veins, transferring oxygen and nutrients to tissues.

Mechanism of Vasoconstriction

• Vasoconstriction is the immediate response to vessel injury, narrowing the blood vessel to reduce blood flow.
• This is triggered by vessel injury (e.g., a cut in a vessel) to reduce blood loss immediately. This is through chemical signals released by platelets and cells.

The Endothelium

• The endothelium, cells lining blood vessels, plays a role in preventing blood clot formation (under normal conditions), as the surface usually repels platelets.
• The extracellular matrix (ECM) interacts with platelets leading to the formation of a platelet plug.

Explore the intricate system of haemostasis and coagulation involving vessels, platelets, and various factors. This quiz covers the balance between thrombosis and haemorrhage, and the mechanisms behind clot formation and removal. Test your knowledge on primary and secondary haemostasis and the physiological aspects of coagulation.