| Thrombosis | formation of a blood clot |
| Embolus | a detached blood clot |
| Coagulation | blood turning into a solid |
| Collagen plus platelet activation causes a platelet plus via what compounds | vWF and fibrinogen |
| To form a blood clot what does factors converts fibrinogen | Thrombin converts fibrinogen to fibrin |
| What does plasmin do | carry out fibrinolysis and clot degradation |
| Platelets carry out what | A haemostatic plus known as primary haemostasis |
| Coagulation is | the formation of a fibrin clot or secondary haemostasis |
| What are some thrombosis activators | vWF, fibrinogen, thrombin, collagen, ADP |
| List some inhibitors of thrombosis | PGI2, NO2, |
| TxA2 is a | prothrombotic eicosanoid |
| What four key fucntions does thrombin carry out | vasoconstriction, fibrin clot formation, coagulation amplification and platelet activation |
| Anti-coagulant | A drug that prevents blood from clotting |
| Anti-thrombotic | A drug that prevents thrombus formation |
| Thrombolytic | A drug that dissolves blood clots |
| In arterial clots what is more critical platelets or coagulation | arterial platelets critical so clot is white |
| Anti-platelet drugs include | aspirin and clopidogrel |
| Venous thrombosis relies on | Cougulation therefore is red |
| Coagulants include | Warfarin and heparin |
| Virshows triad | Blood flow- immobile i.e. atrial fib., endothelial injury- trauma e.g. atherosclerosis and hypercoagulation- inherited, pregnancy or medication |
| aIIbb3 antagonists work via | monoclonal antibody, restricted acute care as risk bleeding low efficacy and higher mortality |
| Aspirin affects | COX which produces TxA2 inhibiting platelet aggregation |
| Clopidogrel | Inhibits platelet adhesion |
| aIIbb3 antagonists | Abciximab- monoclonal antibody |
| P2Y12 inhibitor- very good | Clopidogrel |
| What is warfarin and how does it work | Anti-thrombotic i.e. a blood thinner, works by inhibiting oxy carbolation of coagulation factors in the liver |
| Common anticoagulatns | Heparin- 2 forms, warfarin, Xa and thrombin inhibitors |
| Common clot busters- activate plasmin | Recombinant tPA, e.g. alteplase, reteplase and tenecteplase, urokinases- abbokiase, kinlytic and streoptokinase |
| Primary haemorrhage in dentistry is | Bleeding which occurs during surgery |
| Reactionary haemorrhage | 2-3 hours after surgery |
| Haemostatic agents in dental surgery | passive- Gelatins, collagen etc.. |
| Minor bleeding procedure with anti-coagulant patients | Gelatin sponge, fibrin glue and suture |
| Severe haemorrhage in anti-coagulant patient | Cauterization of soft tissue bleeding |
| HemCon dental dressing | Achieves haemostasis, fastens the wound for healing as +ve atracts -ve RBCs |
| If carry out curretage haemostasis is achieved by | transexamic acid, suture or gelatine sponge and local hemostatic agents |
| Local non surgical interventions | Sealants, adhesives, absorbable agents, biologics and combination products aswell as local anti fibrinolytic agents such as transexamic mouthwash, fibrin glue or adhesive, resorbablel collagen or gelatin sponge |
| Should you ask a patient to stop their anticoagulant | No they could die |
| Systemic interventions for patients with associated cause for bleeding | § administration of fresh frozen plasma (FFP), platelets or both
§ factor replacement therapy, using recombinant or plasma‐derived anti‐haemophilic factor A (FVIII) or anti‐haemophilic factor B or VWF
§ intranasal desmopressin
§ oral or intravenous tranexamic acid
intravenous epsilon amino‐d‐caproic acid |
