Primary Hemostasis PDF

Understanding Primary Hemostasis The First Line of Defense Against Bleeding Kathleen Mae B. Dayoha, RMT, MBA  Primary Hemostasis De nition The initial phase of the complex process by which the body prevents and controls bleeding. It primarily involves the formation...

Understanding Primary Hemostasis The First Line of Defense Against Bleeding Kathleen Mae B. Dayoha, RMT, MBA  Primary Hemostasis De nition The initial phase of the complex process by which the body prevents and controls bleeding. It primarily involves the formation of a temporary "platelet plug" to seal small breaks or injuries in blood vessels. The key components of primary hemostasis include platelets, endothelial cells lining the blood vessels, and certain plasma proteins, notably von Willebrand factor (vWF). fi Primary Hemostasis Importance in preventing bleeding Rapid Response to Injury: Primary hemostasis is the rst line of defense, initiating within seconds of vessel injury. Quick platelet adhesion and plug formation help minimize blood loss promptly. Formation of Temporary Plug: Platelet adherence and activation lead to the formation of a temporary plug at the site of injury. This plug acts as a physical barrier, preventing further blood leakage. Vessel Wall Protection: The platelet plug not only prevents bleeding but also protects the damaged vessel wall from additional harm. fi Primary Hemostasis Importance in preventing bleeding Foundation for Secondary Hemostasis: Primary hemostasis sets the stage for secondary hemostasis, where the coagulation cascade reinforces the platelet plug with a stable brin clot. Prevention of Excessive Bleeding: By quickly forming a plug, primary hemostasis helps prevent excessive bleeding that could lead to complications such as hemorrhage or shock. Maintenance of Hemostatic Balance: The hemostatic process, including primary hemostasis, is nely regulated to achieve an optimal balance between preventing bleeding and avoiding inappropriate clotting. fi fi Primary Hemostasis Process The process begins when blood vessels are injured, causing exposure of collagen bers and other substances beneath the endothelial lining. Platelets are activated and adhere to the exposed surfaces. The interaction between platelets and the sub-endothelial collagen is facilitated by various adhesion molecules, including glycoprotein Ib (GPIb). fi Primary Hemostasis Process Simultaneously, von Willebrand factor, released by endothelial cells and platelets, plays a crucial role in platelet adhesion and aggregation. It helps stabilize the platelet plug by mediating the binding between platelets and the exposed collagen. Primary Hemostasis Process The activated platelets undergo a change in shape and release various substances, such as ADP (adenosine diphosphate) and thromboxane A2, that further activate neighboring platelets and promote their aggregation. This leads to the formation of a temporary plug at the site of injury, which helps prevent excessive bleeding. Primary Hemostasis Primary hemostasis is an essential and immediate response to: vascular injury, forming the foundation for the subsequent steps in the hemostatic process, known as secondary hemostasis and brinolysis, which involve the coagulation cascade and the formation of a stable blood clot. fi Components of Blood Involved in Primary Hemostasis Platelets Endothelial cells Von Willebrand Factor (vWF) Platelets Role and Function Platelets Introduction Platelets also known as thrombocytes, are small, disc-shaped cell fragments found in the blood They are formed in the bone marrow from precursor cells called megakaryocyte. Platelets Structure Microscopic in size, with a diameter of 2-3 um. Lack a nucleus but contain cytoplasmic structure and granules Rich in various substances essential for hemostasis. Platelets Role in Hemostasis 1. Adhesion When a blood vessel is injured, platelets adhere to the exposed collagen bers in the damaged area. Adhesion is facilitated by speci c receptors on the platelet surface. 2. Activation Adhered platelets undergo activation, involving changes in shape and the release of various bioactive substances from their granules. Activation is a crucial step in preparing platelets for aggregation. fi fi Platelets Role in Hemostasis 3. Aggregation Activated platelets adhere to each other, forming aggregates or clumps. This aggregation is essential for the formation of a temporary plug at the site of vascular injury. 4. Secretion of Bioactive Substances Platelets release various substances upon activation, including ADP, serotonin, and thromboxane A2 These substances play a role in amplifying platelet activation and recruitment. Platelets Role in Hemostasis 5. Initiation of Coagulation Cascade Platelets provide a surface for the coagulation cascade to be initiated. They contribute to the conversion of brinogen to brin, strengthening the platelet plug. fi fi Platelets Importance in Primary Hemostasis Platelets are instrumental in the initial response to vascular injury. They form a primary plug at the site of injury, preventing excessive bleeding. Platelets serve as a crucial link between primary and secondary hemostasis, facilitating the progression to the formation of a stable blood clot. Role of ADP and Thromboxane A2 in Primary Hemostasis Role of ADP and Thromboxane A2 In Primary Hemostasis 1. Adenosine Diphosphate (ADP): Source: Released by activated platelets upon exposure to damaged blood vessel surfaces. Function: Acts as a potent signaling molecule in platelet activation. Stimulates further platelet activation and aggregation. Role of ADP and Thromboxane A2 In Primary Hemostasis Mechanism: ADP binds to speci c receptors on the surface of adjacent platelets. Induces a positive feedback loop, enhancing platelet activation and aggregation. Signi cance: Essential for the ampli cation and reinforcement of platelet response. Contributes to the formation of a stable platelet plug at the site of vascular injury. fi fi fi Role of ADP and Thromboxane A2 In Primary Hemostasis 2. Thromboxane A2 Source: Produced by activated platelets, primarily through the action of cyclooxygenase (COX) enzyme. Function: Promotes platelet aggregation and vasoconstriction. Contributes to the stabilization of the platelet plug. Role of ADP and Thromboxane A2 In Primary Hemostasis Mechanism: Thromboxane A2 activates platelets and facilitates their adherence to the site of injury. Enhances the release of ADP, creating a synergistic e ect on platelet activation. ff Role of ADP and Thromboxane A2 In Primary Hemostasis Signi cance: Essential for reinforcing platelet aggregation and maintaining the integrity of the temporary plug. Supports the overall e ectiveness of primary hemostasis in preventing excessive bleeding. fi ff Endothelial Cells and Von Willebrand Factor (vWF) In Primary Hemostasis Endothelial Cells and Von Willebrand Factor in Primary Hemostasis 1. Endothelial Cells: Location: Inner lining of blood vessels (endothelium). Role in Primary Hemostasis: Serve as a physical barrier between blood and tissues. Contribute to the prevention of excessive bleeding by initiating hemostatic responses. Endothelial Cells Functions 1. Vasoconstriction: Upon vessel injury, endothelial cells constrict blood vessels to reduce blood ow, minimizing bleeding. 2. Anti-thrombotic Properties: Produce and release anti-thrombotic substances such as nitric oxide and prostacyclin. Inhibit platelet activation and aggregation, maintaining blood ow. 3. Production of von Willebrand Factor (vWF): Synthesize and release vWF, an essential protein in primary hemostasis. fl fl Endothelial Cells and von Willebrand Factor in Primary Hemostasis 2. von Willebrand Factor (vWF) Structure: Large multimeric glycoprotein Released by endothelial cells and stored in Weibel-Palade bodies. Role in Primary Hemostasis: Facilitates platelet adhesion and aggregation Serves as a carrier for factor VIII in the blood clotting cascade. Von Willebrand Factor Functions 1. Platelet Adhesion: Forms a bridge between platelets and exposed collagen at the site of vascular injury. Enhances the adhesion of platelets to the damaged vessel wall. 2. Stabilization of Factor VIII Binds and stabilizes factor VIII, protecting it from rapid degradation Factor VIII is crucial for the ampli cation of the coagulation cascade. fi Von Willebrand Factor Functions 3. Interaction with platelet receptors Binds to platelet receptors, particularly GPIb, facilitating platelet activation.