Haemostasis - Tagged PDF

Haemostasis Tutor: Gulshana Choudhury Module: Biomedical Sciences GDC Learning outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.6 Describe relevant and appropriate physiology and explain its applica;on to pa;ent management 1.1.8 Describe the...

Haemostasis Tutor: Gulshana Choudhury Module: Biomedical Sciences GDC Learning outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.6 Describe relevant and appropriate physiology and explain its applica;on to pa;ent management 1.1.8 Describe the proper;es of relevant medicines and therapeu;c agents and discuss their applica;on to pa;ent management Learning outcomes Describe the process of haemostasis and clot forma;on Describe the clo?ng cascade and the signi@cance of clo?ng factors Outline the relevance of haemostasis to the dental hygienist/therapist What is haemostasis? I The process by which bleeding stops - insurt When a blood vessel is damaged a number of overlapping processes occur to stop bleeding Why is haemostasis important? Blood is an important connec;ve ;ssue Keeps all organs nourished If we are injured, it is important that blood loss is stopped as quickly as possible Protective Mechanism Consequences of rapid blood loss jur au Larger - Deep Minor loss -smalsure - Moderate loss eg need rose Long Body’s homeostatic mechanisms Headache maintain blood volume and cells Fatigue Nausea Sweating Dizziness can exerience.  Younger and elderly people more at risk Consequences of rapid blood loss severe Injury Severe loss More than 20 % blood loss Clammy, cold, pale skin Rapid, shallow breathing, rapid heart rate Little or no urine output Confusion Weakness Need to be treated in hospital Weak pulse Blue lips and fingernails Light-headedness Can lead to anemia - lead to impacts in the mouth Loss of consciousness Death Stages of haemostasis 3 stages broken into 2 parts 1.Vasoconstriction 2. Platelet plug 3. Coagulation get smaller formation clotting at sight of injury Primary haemostasis Secondary haemostasis Primary haemostasis 1. VasoconstricFon Ini;al bleeding stopped by constricFon of blood vessels Platelets adhere to damaged wall Platelets release serotonin (5-HT) and blood vessels thromboxanes -causes constriction of. Smooth muscle in vessel wall contracts Other vasoconstrictors e.g. endothelins are released by damaged vessel Primary haemostasis 2. Platelet plug Platelets clump together around exposed collagen @bres Process is assisted by a glycoprotein in the blood plasma called von Willebrand factor – stablises platelet plug Platelets release chemicals e.g. adenosine diphosphate (ADP) which aWracts other platelets to site Forma;on of platelet plug Bleeding Fme The ;me taken for primary When is bleeding ;me haemostasis (blood vessel prolonged? conditionsa medication constric;on and platelet plug Thrombocytopaenia, severe forma;on) to occur anaemia, collagen disorders e.g. Ehlers Danlos syndrome, Von Willebrand’s disease 2-7 minutes Anti-platelet drugs e.g. aspirin, clopidogrel  Made up of white blood cells, red blood,cells, platelets, fibrin Secondary haemostasis 3. CoagulaFon Platelets Red/white blood cells Complex process resul;ng in Fibrin platelet plug being stabilised by insoluble @brin strands forming a mesh Clot Fibrin is formed from the soluble @brinogen through the clo?ng cascade Fibrin mesh Built up of fibers and stabilises the clot that’s built up of platelet plug. CloKng cascade 3 pathways , intrinsic , extrinsic , common pathway Number of cloting factors reflects the order in which they where discovered and not necessarily they order they work in. Extrinsic pathway (Fssue factor pathway) As soon as injury occurs this tissue factor is realised, this factor coverts factor 7 Main pathway to factor 7a. Triggered by Tissue factor (factor III) released by damaged Factor 7/ VIIa activates factor 10/ X into factor endothelial cells 10a / Xa Tissue factor converts factor VII to factor VIIa Factor 7 /VII is inactive state Factor 7a / VIIa activated state Factor VIIa goes on to ac;vate factor X into factor Xa Extrinsic Pathway Therea_er common pathway measured by Prothrombin Time (PT) Normal value = 11-16 seconds  to blood vessel wall. something happening - Intrinsic pathway (contact pathway) and slower Longer pathway. Triggered by blood coming into contact with collagen @bres in the broken wall of a blood vessel S “Intrinsic" because it's ini;ated by a factor inside the blood vessel Starts with ac;va;on of factor XII (serine protease) which becomes factor XIIa a_er exposure to Intrinsic Pathway measured endothelial collagen a_er damage. by Activated Partial Thromboplastin Time Ends with common pathway (aPTT) Normal value = 23-35 seconds Common pathway Prothrombin is converted to thrombin (serine protease) Factor 10 / x converts to factor 10a/ xa Thrombin converts the soluble @brinogen into @brin strands Factor XIII acts on @brin strands to form a @brin mesh CoagulaFon factors Majority are synthesised in the liver Factor VII is created by the vascular endothelium Vit K essen;al for forma;on of clo?ng factors in the liver Liver pathology can cause problems with forming clo?ng factors hi e Inherited disorders such as Haemophilia A, B and C lead to a lack of factor VIII, IX and XI respectively 8911  preventblood o a in - EQects of anFcoagulants on the cloKng cascade Anticoagulan Indications: ts are drugs Atrial that help 8brillation prevent Deep vein blood from thrombosis clotting Stroke sed increaseding Drisk : Drugs such as Warfarin, Heparin and Rivaroxaban block different parts of the clotting cascade Summary of the coagulaFon cascade tracted factor. plattesSe. -Tissue released Clot retracFon Contrac;on of approximately 90% of ini;al clot volume within 24 hours Ac;n and myosin proteins within ac;vated platelets pull clot ;ght Fibrin threads draw more closely together Serum exudes Clot shrinkage pulls the edges of the damaged vessel together, reducing blood loss Clot breakdown – Tbrinolysis Plasminogen, trapped within the clot is converted to plasmin Enzyme - Plasmin breaks down @brin Thrombin ac;vated @brinolysis inhibitor (TAFI) is a @brinolysis inhibitor and stabilises clots I Levels PT Reduced in with heamophilia. Fibrinolysis – abnormaliFes Fibrinolysis enhanced by Fibrinolysis depressed by Disseminated intravascular Alcoholic liver disease coagulation Antiphospholipid syndrome Metastatic prostate cancer Hypothyroidism Sepsis Chronic renal disease trauma Pregnancy Severe concer  Blood clot Thrombosis - Caused by: 1. Over-ac;vity of coagula;on 2. Under-ac;vity of @brinolysis Most o_en starts at an area of vascular endothelial damage to which platelets adhere Dental relevance Dental procedures cause haemorrhage Bleeding should stop naturally a_er 4-10 min depending on wound Separate lecture on the many causes of prolonged bleeding and how to manage it Haemorrhage in denFstry Controlled in den;stry by: Pressure Sutures Packing with haemosta;c agents e.g. Surgicel Less commonly: Electrosurgery unit – coagula;on wavelength Lasers Summary Described the process of haemostasis and clot forma;on Described the clo?ng cascade and the signi@cance of clo?ng factors Briejy described clot retrac;on and @brinolysis Outlined the relevance of haemostasis to the dental hygienist/therapist Quiz hWps://forms.okce.com/e/4Gwp2jucNm Further reading Haemostasis revealed. Available at: hWps://www.youtube.com/watch?v=-F73CMjVuqg Haemostasis revealed. Available at: hWps://www.youtube.com/watch?v=-F73CMjVuqg SDCEP Management of Dental Pa.ents Taking An.coagulants or An.platelet Drugs (second edi.on) 2022. Available at hWps://www.sdcep.org.uk/media/ypnl2cpz/sdcep-management-of-dental- pa;ents-taking-an;coagulants-or-an;platelet-drugs-2nd-edi;on.pdf