The coagulation cascade is shown, separated into different phases with their endogenous and pharmacological inhibitors shown. During the initiation phase, small amounts of FXa is generated by Tissue Factor exposure at the site of injury. TF complexes with FVIIa generating FXa which itself complexes with FVa to generate thrombin (extrinsic pathway). TF-FVIIa also activates FIX along with FXIIa (intrinsic pathway). Thrombin, then primes additional multicomponent complexes on platelets (and endothelial cells, not shown) (amplification phase). Once activated the multicomponent complexes are optimally positioned to generate large amounts of thrombin (propagation phase).
#Coagulation#Cascade#platelet#thrombin#clot#PT#PTT#diagnosis#models#hematology#pathophysiology#anticoagulation#anticoagulant#Warfarin#Dabigatran#thrombin#inhibitor#Apixaban#Rivaroxaban#Edoxaban#heparin#pathway
Currently, I am a medical student at Drexel University College of Medicine, Class of 2024. My ambition is to become a physician-scientist and I look forward to continuing my training acquiring the full suite of research and clinical capabilities so that I can improve lives both at the bench and the bed side.
My current research interests involve gaining a superior understanding of the interplay between hematology and immunology by investigating the role platelets as members of the innate immune system and their functions in immune-mediated pathologies
