Platelets and Hemostasis PDF
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Uploaded by UnlimitedErbium
Gulf Medical University
2024
Dr.Rasha Eldeeb
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Summary
This is a lecture presentation on platelets and hemostasis, suitable for an undergraduate or postgraduate medical or physiology course, covering aspects like platelet function, hemostatic mechanisms, and disorders. It was given at Gulf Medical University on September 24, 2024.
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Platelets and Hemostasis Dr.Rasha Eldeeb Associate Professor of Physiology September 24, 2024 1 www.gmu.ac.ae COLLEGE OF PHARMACY ...
Platelets and Hemostasis Dr.Rasha Eldeeb Associate Professor of Physiology September 24, 2024 1 www.gmu.ac.ae COLLEGE OF PHARMACY Platelets and Hemostasis Learning Objectives: Define Platelets Describe platelet's structure and relate that to its function Desrcibe the variation in Platelets count Define Haemostasis Explain the mechanisms of Haemostasis Describe the fibrinolytic system Describe the disorders of Hemostasis What is Platelet? Platelets (Thrombocytes) are minute discs 1 to 4 micrometers in diameter They are formed in the bone marrow through the Myeloid pathway from megakaryocytes, which are extremely large cells of the hematopoietic series in the marrow The megakaryocytes fragment into the minute platelets either in the bone marrow or soon after entering the blood, especially as they squeeze through capillaries The normal concentration of platelets in the blood is between 150,000 and 400,000 per microliter with an average of 250,000/ul. What is the function of the Platelet? When platelets come in contact with a damaged vascular surface, especially with collagen fibers in the vascular wall, the platelets immediately begin to swell; assume irregular forms with numerous irradiating pseudopods protruding from their surfaces Their contractile proteins contract forcefully and cause the release of granules that contain multiple active factors They become sticky so that they adhere to collagen in the tissues and to a protein called von Willebrand factor that leaks into the traumatized tissue from the plasma They secrete large quantities of ADP; and their enzymes form thromboxane A2 both in turn act on nearby platelets to activate them as well, and the stickiness of these additional platelets causes them to adhere to the original activated platelets Therefore, at the site of any opening in a blood vessel wall, the damaged vascular wall activates successively increasing numbers of platelets that themselves attract more and more additional platelets, thus forming a platelet plug This is at first a loose plug, but it is usually successful in blocking blood loss if the vascular opening is small Then, during the subsequent process of blood coagulation, fibrin threads form. These attach tightly to the platelets, thus constructing an unyielding plug Normally Platelets do not stick to each other or to the endothelial lining of blood vessels (Intact endothelium secret prostacyclin and NO which inhibit aggregation) The Platelets Functions in Hemostasis: 1. Release of vasoconstrictors to cause vessel spasm 2. Formation of platelet plug 3. Facilitates blood coagulation by the release of clotting factors like platelet factor 3 4. Causes clot retraction 5. Repair of damaged tissue by the release of PDGF (platelet derived growth factor) What are the variations in Platelets count? Thrombocytopenia purpura is a condition where platelet counts are lower than normal, potentially leading to mild to serious bleeding. This bleeding can happen inside the body (internal bleeding) or on the skin Several factors can cause a low platelet count, such as: o The bone marrow doesn't make enough platelets o The bone marrow makes enough platelets, but the body destroys them (autoimmunity) or uses them up o The spleen holds onto too many platelets. The spleen is an organ that normally stores about one- third of the body's platelets o A combination of the above factors Thrombocytosis is a condition where platelet counts are higher than normal. Several factors can cause a high platelet count, such as: o Chronic inflammatory disorders o Malignant disease o Tissue damage o Hemolytic anemias o Post- splenectomy o Post –hemorrhage o Chronic myeloid leukemia What is Hemostasis? Stoppage of bleeding by forming blood clots in the wall of damaged blood vessels, meanwhile the rest of the blood is maintained in a fluid state within the vascular system The Mechanism: grl-stop-sign A. Local Vasoconstriction B. Temporary hemostatic plug Formation (platelet reaction) C. Definitive hemostatic plug formation ( Blood Coagulation) D. Repair of damaged blood vessel Clotting Mechanism ( Blood Coagulation) How is the Rest of the Blood is Kept in a Liquid State? Fibrinolytic System The liver produces an inactive globulin called plasminogen (profibrinolysin). This can be converted to an active enzyme called plasmin (fibrinolysin) by thrombin and tissue plasminogen activator (tPA) which is released from injured tissues and vascular endothelium Plasmin lyses fibrin into fibrin degradation products (FDP) which inhibit thrombin The liver also produces a tPA inhibitor (antiplasmin), which delays fibrinolysis What Are The Disorders of Hemostasis? Vitamin K deficiency : This leads to hemorrhage due to inhibition of formation of prothrombin and factors VII, IX & X in liver. Hemophilia : It is a hereditary sex linked recessive hemorrhagic disease transmitted by females (who are not affected but act as carriers) to males (who are affected) Learning Resources: Marieb EN. Human Anatomy and Physiology, 9th Edition, Pearson International Edition; 2014. ISBN-13: 978-1-2920-2649-7 Guyton, Arthur C. Textbook of medical physiology / Arthur C. Guyton, John E. Hall.—11th ed. Ganong's Review of Medical Physiology/Kim E. Barrett, Susan M. Barman, Scott Boitano and Heddwen L.Brooks,23rd ed. Instructional Web site Lectures PDF on Moodle https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780702031144000026 DISCLAMER The contents of this presentation, can be used only for the purpose of a Lecture, Scientific meeting or Research presentation at Gulf Medical University, Ajman. www.gmu.ac.ae