Primary Hemostasis Lecture - 1 PDF

Primary Hemostasis Lecture - 1 Haemostasis or Hemostasis ‫بأنه توقف النزيف من األوعية الدموية‬ ❖Hemostasis can be defined as the stoppage of bleeding from the blood vessels ❖It is a complex process in which several factors work together or in sequence to stop the flow of blood from an in...

Primary Hemostasis Lecture - 1 Haemostasis or Hemostasis ‫بأنه توقف النزيف من األوعية الدموية‬ ❖Hemostasis can be defined as the stoppage of bleeding from the blood vessels ❖It is a complex process in which several factors work together or in sequence to stop the flow of blood from an injured blood vessel. ❖The five major components of normal hemostasis are platelets, coagulation factors, coagulation inhibitors, fibrinolysis and blood vessels.  ‫ يتم الحفاظ على تكوين وانحالل الخثرات الدموية في توازن دقيق‬،‫ظل الظروف العادية‬ Under normal conditions, the formation and dissolution of thrombi is maintained in a delicate balance (‫وبدون هذا التوازن قد يتعرض الفرد إما لنزيف شديد أو انسداد األوعية الدموية )تجلط الدم‬ Without this balance, the individual may experience either excessive bleeding or Vaso- occlusion (thrombosis) Hemostasis can be divided into two stages: 1- Primary 2- Secondary. - Primary hemostasis includes the platelet and vascular response to vessel injury. - Secondary hemostasis includes the coagulation factors response to such injury. Megakaryocyte and platelets formation Platelets Site of formation: (Bone marrow) Myeloid stem cell Megakaryoblast Megakaryocyte Platelets Platelets (Thrombocytes): They are fragments of megakaryocytes formed in the bone marrow. Their production (thrombopoiesis) is regulated by Thrombopoietin, a hormone released from the liver. Platelets Are round/oval disc with diameter about 2-3 μm. Coated by a glycoprotein layer which prevents their sticking to normal endothelial cells. Platelet count = 250,000-500,000/ mm3. life span 8-12 days. Active cells contain contractile protein such as actin, myosin, and thrombosthenin. Contain high calcium content & rich in ATP.  Platelet production: Platelets are produced in the BM by fragmentation of the cytoplasm of megakaryocytes, one of the largest cells in the body. The precursor of the megakaryocyte-the Megakaryoblast-arises by a process of differentiation from the haemopoietic stem cell. The megakaryocyte matures by endomitotic synchronous replication) enlarging the cytoplasmic volume as the number of nuclear lobes increase in multiples of two. approximately each megakaryocyte giving rise to 1000-5000 platelets. Hemostasis: prevention or stoppage of blood loss. Hemostatic Mechanisms: 1.Vessel wall (Vasoconstriction) 2.Platelets (Production and activation, Platelets Plug formation) 3.Blood coagulation. Clot formation (intrinsic & extrinsic pathways) 4. Fibrinolysis Hemostatic Mechanisms: Vessel wall Immediately after injury, there is a localized Vasoconstriction of smooth muscles. Mechanism -Hormonal factors: local release of thromboxane A2 & serotonin (5HT) from platelets Systemic release of adrenaline - Nervous reflexes (pain nerve impulses) Platelet Functions Begins with Platelet activation. Adhesion Shape change Aggregation Release Clot Retraction Platelet Adhesion Platelets stick to the exposed collagen underlying damaged endothelial cells in vessel wall. Platelet shape change and Aggregation. Platelet Aggregation Activated platelets stick together and activate new platelets to form a mass called a platelet plug. Plug reinforced by fibrin threads formed during clotting process. Platelet Release Reaction Platelets activated by adhesion. Extend projections to make contact with each other platelets. Release thromboxane A2, serotonin & ADP activating other platelets. Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel. ADP causes stickiness. Platelet plug formation Platelet Plug Aggregation of platelets at the site of injury to stop bleeding. Exposed collagen attracts platelets. Activated platelets release ADP & Thromboxane A2 (TXA2) the stickiness of platelets Platelets aggregation plugging of the cut vessel Intact endothelium secretes Prostacyclin inhibition of aggregation Activated Platelets Secrete: 1. 5Hydroxytryptamine(5HT) vasoconstriction 2.Platelet phospholipid Factor (PF3) clot formation 3.Thromboxane A2 (TXA2) is a prostaglandin formed from Arachidonic acid Function: Vasoconstriction Platelet aggregation (TXA2 inhibited by aspirin)