Hematology: Hemostasis

• Platelets are also called thrombocytes and maintain hemostasis.
• Platelets are cell fragments shed from megakaryocytes.
• Megakaryocytes are large bone marrow cells that produce platelets.
• Platelets are functional for 7-10 days and are removed from circulation by macrophages.
• 1/3 of platelets are stored in blood-filled spaces in the spleen.
• Thrombopoietin stimulates the bone marrow to make more platelets.
• Hemostasis is the process of stopping blood loss.
• Hemostasis is rapid and localized, with the main goal being an equilibrium between bleeding and clotting.
• When the body stops bleeding and maintains blood as fluid in its vessels, it is in hemostasis.
• The main steps of hemostasis are 1. Vascular spasm (aka vasoconstriction) 2. Formation of a platelet plug, and 3. Coagulation (clot formation)
• The vessel wall provides a physical barrier between circulating thrombocytes and highly thrombogenic collagen.
• Healthy endothelial cells produce nitric oxide and prostacyclin, which are vasodilators and prevent platelet adhesion.
• Endothelial cells are the primary producers of Von Willebrand Factor (VWF).
• When damage to blood vessels occur, prostacyclin and nitric oxide are not released from the endothelial cells, causing vasoconstriction and platelet aggregation.
• Damaged endothelial cells of the vessel release Von Willebrand Factor
• VWF is attracted to the exposed collagen and forms a bridge between the platelets and the injured tissue. VWF can be thought of as a glue.
• Platelets have surface glycoprotein IIbIIIa that undergoes a conformation change under platelet activation.
• After vasoconstriction and platelet adhesion to injured site, platelets in the aggregation stage attach to collagen and are activated.
• The shape change of GP IIb-IIIa of the platelets allows fibrinogen to attach to platelets.
• Degranulation occurs during the aggregation phase of platelet plug formation, and serotonin, ADP, and Ca 2+ are released.
• Serotonin causes vasoconstriction and smooth muscle contraction.
• ADP stimulates more platelet degranulation and attracts more platelets to the injury site.
• Calcium helps in the coagulation cascade, serving as a cofactor for several clotting factors.
• Fibrinogens are proteins that attach to platelets and link them together, helping them form a clot at an injury site.
• Platelet plugs are unstable, but can be stabilized through coagulation and clot formation.
• Blood clots have a fibrin mesh across platelets but plugs don't.
• During primary hemostasis, platelets clump up together and form a plug around the site of injury.
• In secondary hemostasis, a fibrin mesh stabilizes the platelet plug and forms a clot.
• The goal of the coagulation cascade is to convert fibrinogen into fibrin.
• Fibrinogen is a zymogen, meaning its an inactive protein that must be cleaved to be activated.
• Without coagulation, a platelet plug will break apart within 24 hours.
• There are 12 coagulation factors named with roman numerals.
• The coagulation factors are numbered 1-13 except 6 was removed upon further research.
• Factor I is fibrinogen.
• Factor II is prothrombin.
• Factor III is tissue factor.
• Factor IV is calcium (cofactor).
• Factor V is labile factor (cofactor).
• Factor VII – factor XII are unnamed for our purposes.
• Factor XIII is fibrin stabilizing factor.