SEARCH RESULTS FOR: Primary-Hemostasis

Primary Hemostasis

Primary Hemostasis: Normal physiology, disorders, and clinical findings Authors: Mina Mina Reviewers: Parker Lieb Mao Ding Kareem Jamani* *MD at time of publication Normal physiology: Injury to blood vessels from trauma (blunt or penetrating injury) Disorders of primary hemostasis: Collagen and microfibrils (subendothelial elements that are normally protected) are exposed to circulating blood due to vessel injury Storage granules in endothelial cells release large multimers of clotting factor von Willebrand (vWF) when damaged Acquired or inherited reduction in vWF quantity or quality (see vWF deficiency slide) von Willebrand Disease Defect in expression of GpIb interferes with platelet ability to bind to vWF Bernard-Soulier syndrome Defect in platelet membrane glycoproteins IIb and IIIa Glanzmann’s Thrombasthenia Insufficient platelets to form a platelet plug Thrombocytopenia (low platelet count) Disorders of primary hemostasis: problems with formation of a platelet plug Platelet adhesion: vWF binds to collagen and interacts with the platelet surface receptor glycoprotein Ib (GpIb) allowing platelet adhesion Platelet activation: mediated by agonists like ADP, thrombin and collagen Mucocutaneous bleeding (bleeding of the skin and mucous membrane) ↑ Closure time, ↑ bleeding time Platelets change shape and release substances from their granules Conformational changes in platelet cell surface glycoprotein IIb/IIIa ↑Affinity for fibrinogen through GpIIb/IIIa ADP Fibrinogen, vWF, and other substances Thromboxane A2 (see note) Induces aggregation Epistaxis Menorrhagia Note: Petechiae Platelet aggregation: fibrinogen forms bridges between adjacent platelets by binding to activated glycoprotein IIb/IIIa Interaction with coagulation factors: platelets provide a scaffold that allows the activation of phospholipid-dependent coagulation factors Primary hemostasis (formation of a platelet plug) Secondary hemostasis (see slide for normal physiology) Drugs like Aspirin and NSAIDs inhibit Thromboxane A2 synthesis (by inhibiting cyclooxygenase) and thereby inhibit platelet aggregation Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published March 30, 2023 on www.thecalgaryguide.com