Haemostasis GN 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? The process by which bleeding stops When a blood vessel is damaged a number of overlapping processes occur to stop bleeding Cut or injury Cellular level - A number of processes have to occur in order for bleeding to stop Dental - PMPR - causes bleeding After extraction, blood pools into sockets, after a few minutes of pressure the bleeding should stop. 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 As a protective mechanism  Consequences depend on severity of blood loss Consequences of rapid blood loss Small on cellular level, small injuries. Minor loss Moderate loss Result of deep cut, internal or external bleeding, consistent nose bleed. Body’s homeostatic mechanisms Headache maintain blood volume and cells Fatigue Nausea Sweating Dizziness Consequences of rapid blood loss Hypovolemic shock More than 20% of blood has been lost. Severe loss Young children and elderly usually most vulnerable. Consequences and signs can be severe. Clammy, cold, pale skin Rapid, shallow breathing, rapid heart rate Little or no urine output Confusion Weakness Weak pulse Body is starting to shut down Blue lips and fingernails Body prioritised blood supply to organs (brain) Causes blue skin/lips Light-headedness Loss of consciousness Usually have to treated into hospital Death Likely to have blood transfusion Can also lead to anaemia - can affect oral cavity. Anaemic - consideration for treatment due to increased risk of bleeding Stages of haemostasis 1.Vasoconstriction 2. Platelet plug 3. Coagulation formation Primary haemostasis Secondary haemostasis Platelet formation - help form clot at sight of injury Injury - blood vessels constrict (smaller) One of the first cells attracted Less blood can be lost due to constructed vessels Platelets attract more platelets Primary haemostasis 1. VasoconstricFon Vasoconstriction is what essentially will stop the blood going through vessel walls. Ini;al bleeding stopped by constricFon of blood vessels When platelets come into contact with damaged blood vessels, their surface becomes sticky and they stick to damaged blood vessels wall. Platelets adhere to damaged wall Platelets release serotonin (5-HT) and These also constricts blood vessel thromboxanes Protective mechanisms in place to save body and prevent body from loosing more blood. Smooth muscle in vessel wall contracts Other vasoconstrictors e.g. endothelins are released by damaged vessel  Formation of platelet plug Platelets at sight of injury attract more platelets to come together around exposed collagen Primary haemostasis fibres. Protein - von Willebrand factor - stabilises platelet plug ADP attract more platelets to help form platelet plug. 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  Need to take accurate medical history to know about bleeding risk of patient. Bleeding Fme The ;me taken for primary When is bleeding ;me haemostasis (blood vessel prolonged? Certain conditions and medications constric;on and platelet plug Thrombocytopaenia, severe forma;on) to occur anaemia, collagen disorders e.g. Ehlers Danlos syndrome, Von Usually = Willebrand’s disease 2-7 minutes Anti-platelet drugs e.g. aspirin, clopidogrel 1. Vasoconstriction - primary 2. Platelet plus - primary 3. Coagulation - secondary Secondary haemostasis 3. CoagulaFon Clot is made up of 4 components 1. Platelets 2. Red/white blood cells 3. Fibrin 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 Build up of fibres together - stabalises clot forming from platelet plug.  CloKng cascade Secondary haemostats 3 pathways Intrinsic - Extrinsic - Feed into common pathway. Numbers of clotting factors reflect order in which they were discovered, NOT the order they work in. Extrinsic pathway (Fssue factor pathway) Main pathway By which coagulation cascade is activated. Triggered by Tissue factor (factor III) released by damaged endothelial cells As soon as you injure yourself the tissue factor is released (FACTOR III) Tissue factor converts factor VII Factor 7 = inactive state Factor 7a = activated state to factor VIIa 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  Longer and slower pathway in secondary haemostasis Intrinsic pathway (contact pathway) Extrinsic - most common due to tissue factor being released after injury Intrinsic- initiated INSIDE blood vessel wall Triggered by blood coming into contact with collagen @bres in the broken wall of a blood vessel “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  Both extrinsic and intrinsic pathways both fall into common pathway after activation be certain coagulation factors. Begins at factor 10 - activated into factor 10a Common pathway Factor 12 acts on fibrin strands to help form fibrin mesh to keep secure and stabilise. Prothrombin is converted to thrombin (serine protease) Thrombin converts the soluble @brinogen into @brin strands Factor XIII acts on @brin strands to form a @brin mesh -  Clotting CoagulaFon factors Majority are synthesised in the liver 7 Factor VII is created by the vascular endothelium Vit K essen;al for forma;on of clo?ng factors in the liver Can include alcohol issues Liver pathology can cause problems with forming clo?ng factors May want to get patients blood levels checked before extractions to ensure levels are correct for limited bleeding complications.  Coagulation Inherited disorders such as Haemophilia A, B and C lead to a lack of factor VIII, IX and XI respectively 8, 9, 11 Higher bleeding risk - treated in hospital  EQects of anFcoagulants on the cloKng cascade Anticoagulan Indications: ts are drugs * Atrial that help 8brillation prevent B Deep vein blood from thrombosis clotting & Stroke Different medications - Target clotting cascade in different ways. Effect bleeding risk. Need to consider dental treatment. Drugs such as Warfarin, Heparin and Rivaroxaban block different parts of the clotting cascade  Summary of the coagulaFon cascade 1. Initial injury - damaged blood vessel wall, blood can escape into surrounding tissue. 2. Vasoconstriction - tissue factor released, smooth muscle constricts to reduce blood flow. 3. Platelet plug formation - platelets adhere, stick to each other to form temporary seal. More platelets attract to more platelets. 4. Fibrinogen converted into mesh of fibrin by thrombin. Stabalises and strengthens clot. 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  The clot does need to break down once the body does a period of healing. 1st step - break down of fibrin Clot breakdown – Tbrinolysis Plasminogen, trapped within the clot is converted to plasmin (Enzyme) By activators released by damaged cell walls. Plasmin breaks down @brin Thrombin ac;vated @brinolysis inhibitor (TAFI) is a @brinolysis inhibitor and stabilises clots Clot will break down. Fibrinolysis – abnormaliFes Fibrinolysis enhanced by Fibrinolysis depressed by Disseminated intravascular Alcoholic liver disease coagulation Antiphospholipid syndrome Metastatic prostate cancer Hypothyroidism Where systemic inflammation (sepsis, Chronic renal disease severe trauma), results in increased consumption of fibrin within blood vessels. Pregnancy Causes deficiency. Formation of a blood clot inside blood vessel, can block blood flow. Thrombosis Caused by: More clots 1. Over-ac;vity of coagula;on 2. Under-ac;vity of @brinolysis Once clot forms, the clot doesn’t break down. Most o_en starts at an area of vascular endothelial damage to which platelets adhere Anywhere there is damage in the system Dental relevance PMPR BPE Extraction Dental procedures cause haemorrhage Bleeding should stop naturally a_er 4-10 min depending on wound And patient Separate lecture on the many causes of prolonged bleeding and how to manage it Medications can increase risk of bleeding - risk assessment needed to be taken for these patients. Haemorrhage in denFstry Controlled in den;stry by: Pressure Gauze, biting together to stop blood flow and reduce blood loss. Sutures If blood flow not stopped with pressure. Packing with haemosta;c agents Before suturing 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 Clot breakdown Briejy described clot retrac;on and @brinolysis Outlined the relevance of haemostasis to the dental hygienist/therapist How to control bleeding/haemostasis 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