Teaching /DIC Images! Clots Widespread !
Channel: Marie M Francois Pierre-Louis
Date: 2019-01-26

Invite people to have values such as patience, to build faith and hope and love for each other.DIC Disseminated Intravascular coagulation, characterized by systemic activation of blood coagulation which results in generation and deposition of fibrin leading to microvascular thrombi and contributing to multiple organ dysfunction. Normal hemostasis as process to make the bleeding stop, is using  reflex vasoconstriction, platelet activation and coagulation cascade, resulting in formation of blood clot. Damage in blood vessels triggers the release of clotting factors. Platelets activated and with vasoconstriction helping, a sticky blue coming. fibrin stands adhere to the plug to form an insoluble clot. Coagulation has 3 stages, platelets attaching to wall, platelets releasing fibrin and begin sealing, fibrin network trapping RBC to complete the seal. In intrinsic pathway, platelets activation and in extrinsic pathway release of tissue factor such thrombin, fibrin. In intrinsic pathway, damage to the vessel wall, a cascade of clotting  going on. Factors went from inactive form to activated form. In extrinsic pathway damage to the tissue outside the vessel. Extensive endothelial damage initiates the clotting process, thrombi came in different side than plasmin. With thrombi platelets activated. In micro-circulation trouble due to DIC features. From too many thrombi, ischemia came leading to organ failure. Platelets trouble leads to thrombocytopenia meaning excessive bleeding. From injury in intrinsic pathway, tissue factor activation, and from generation of thrombi, platelets consumption, then thrombocytopenia, more bleeding is coming. In extrinsic pathway, tissue destruction, tissue factor as stimulus in activation, thrombin generation triggering intra-vascular fibrin deposition, then anemia is coming with tissue ischemia. Pro-inflammatory action shut down fibrinolysis, then impairement of natural anti-coagulant pathways. with inflammatory cells receptors, fibrinogen conversion to fibrin, see fibrin-platelet clots. Inflammation with thrombin generation platelets activated. DIC systemic thrombo-haemorrhagic disorder with features such as activation of coagulation and fibrinolytic system, clotting factors in consumption as well natural inhibitors, then thrombocytopenia. Excessive thrombin release meaning disproportionate consumption of factors compromised endothelial barrier more leading to vascular leakage and edema. with Thrombi in small blood vessels, ischemia occurs that can re-trigger the DIC until multiple organ failure. Inflammation involved in DiC which features as extra-vascular fibrin, vascular occlusion by fibrin, inflammatory response, and tissue necrosis until multiple organ failure. From trauma, sepsis and toxin, initiating platelets aggregation leading to vascular occlusion and thrombocytopenia until bleeding. Platelets into coagulation,platelets depleted leading to bleeding. With Fibrin deposited, plasmin initiated as thrombin inhibitor leading to platelet function depleted until bleeding. With fibrin , a decrease in fibrinogen leading to bleeding, fibrin stops to polymerize leading to more bleeding. DIC with uncontrolled thrombin generation , coming fibrin deposit in microcirculation, then platelets in consumption as coagulation factors. Red blood cells RBC damaged. Check vessel patency. Make a diagnosis of DIC with the Test d-Dimer:  positive indicates fibrin deposition from widespread thrombus formation. Diffuse building in area! Excess thrombin in DIC leads to low platelets! From serious medical condition apparition of pro-coagulants TF leading to formation of new clots in one side and fibrinolysis involved in the other side. Plateles activated form a plug. Anti-platelets drug make platelets less able to stick together.Blood-clotting reacts with Proteins in network trapping platelets to make the clot stronger. In coagulation blood changes from liquid to a gel, forming a clot. Bacteria as causative agent in sepsis and endothelial damage initiating coagulation; bacteria with hyperactive immune response as inflammation in triggering coagulation, DIC in coming with tissue damage , organ failure and edema. From tissue factorTF to thrombin to fibrin to formation of clots! Derangement of hemostasis occurs with patients with severe liver disease.in favor of thrombosis, platelet adhesion held together by fibrinogen. Clotting factors tested as PT test and aPTT test. Starting time of blood coagulation to measure!