Bleeding Disorders (Part 1) GN PDF

Bleeding Disorders (Part 1) Biomedical Sciences Dr Anisha Desai 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 application to patient management 1.2.4 Recognise abnormalities of...

Bleeding Disorders (Part 1) Biomedical Sciences Dr Anisha Desai 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 application to patient management 1.2.4 Recognise abnormalities of the oral cavity and the rest of the patient and raise concerns where appropriate 1.5.4 Identify where patients’ needs may diCer from the treatment plan and refer patients for advice when and where appropriate 1.7.2 Explain the impact of medical and psychological conditions in the patient 1.7.9 Recognise local referral networks, local clinical guidelines and policies 1.10.1 Recognise the responsibilities of the dental team as an access point to and from wider healthcare 1.10.3 Underpin all patient care with a preventive approach that contributes to the patient’s long- term oral health and general health 1.11.2 Explain and take account of the impact of the patient’s periodontal and general health on the overall treatment plan and outcomes Aim of the Session Describe bleeding disorders for the dental hygienist/therapist Source: https://bleedingdisordersnc.org/wp-content/uploads/2021/11/iStock-10 57632348-471x484.jpg Intended Learning Outcomes At the end of this session, you should be able to: Refresh knowledge of haemostasis Classify bleeding disorders Recognise medical conditions and drug therapies that alter bleeding risk Haemostasis The normal physiological response that prevents signiXcant blood loss after vascular injury Events: 1. Vascular system – injured vessel initiates vasoconstriction 2. Platelet system – activation and aggregation of platelets to help form plug 3. Activation of the coagulation cascade – to produce Xbrin plug Or stable clot Aggregation of Platelets https://www1.wfh.org/publications/Xles/pdf-1336.pdf Platelets within blood are activated locally which results in increased tendency to adhere and stick to each other and damaged blood vessel — primary haemostasis  Fibrin stabilises the primary platelet plug by cross linking the platelets The Coagulation Cascade together and to damaged blood vessel wall to prevent blood loss - secondary haemostasis ClassiXcation of Bleeding Disorders  Disorders of blood vessels Very rare  Disorders of platelets  Disorders of coagulation Disorders of Blood Vessels Disorders of Blood Vessels Very rare Skin Bruises easily More fragile blood vessels that can bulge or tear Inherited: Hypomobility of fingers and toes Delayed wound healing Connective Tissue Disorders e.g. Ehlers-Danlos Syndrome Genetic Hereditary haemorrhagic telangiectasia (HHT) Affects blood vessels Blood vessels not developed properly and cause bleeding Chronic nose bleeds usually first signs May result in abnormalities affects brain, spinal cord, lungs, liver Acquired: Severe infections: meningococcal, typhoid Results in internal bleeding Drugs: sulphonamides And diuretics Other: Vitamin C deXciency, senile purpura Dark patches of skin  Important for primary haemostasis Disorders of Platelets Disorders of Platelets Acquired conditions more common Thrombocytopenia Idiopathic Thrombocytopenia Purpura (ITP) Liver disease Renal disease Chemotherapy (received less than 3 months ago) Radiotherapy (total body irradiation less than 6 months ago) Connective Tissue Disorders e.g. Ehlers-Danlos Syndrome Rare e.g. Bernard Soulier disease, Jacobsen syndrome, Lowe syndrome Antiplatelet drugs Thrombocytopenia Reduced platelet count: below 150 x 109/L (usual range 150-450 x 109/L) May be due to: Decreased/failure of platelet production Destruction of circulating platelets Disorders of platelet function Idiopathic Thrombocytopenia Purpura (ITP) A rare autoimmune blood disorder that both children and adults can develop, where the immune system attacks the body's own platelets by mistake, most commonly as a result of antibody production against platelets. There are 2 forms of ITP: Acute: arising post-virally (e.g. chickenpox) in children. Self limiting, more common form. Chronic: this disorder can happen at any age. Symptoms can last from 6 months to a lifetime.  Key group of patients to be aware of Liver Disease Increased bleeding risk Reduced platelet numbers but may also have reduced coagulation factors. The liver plays a major role in haemostasis as: It produces coagulation factors such as Factors I, II, VII, IX, X and XI. Failure of normal function of the liver can lead to malabsorption of fat soluble vitamins, such as vitamin K, which is required for the synthesis of blood-clotting factors. Both PT and APTT are prolonged in chronic liver disease Alcohol misuse is one of the causes of liver disease Alcohol can prolong bleeding time produced by aspirin and NSAIDs Post-operative bleeding may occur in alcohol-dependent patients due to: Liver cirrhosis leading to decreased production of clotting factors; Bone marrow suppression and folate deXciency causing thrombocytopenia; Malnutrition due to heavy drinking which can decrease synthesis of  Kidneys play vital role in excreting waste products and maintaining fluid and electrolyte balance Renal Disease Produce hormone erythropoietin - stimulates red blood cell produced in bone marrow and vit D Haemostasis is impaired in patients with chronic renal failure owing to:  Impaired platelet production  Impaired platelet adhesion  A decrease in platelet factor 3  Vasodilation  Haemodialysis patients (chronic renal failure) taking heparin Clinicians may need to be aware of signs and symptoms of renal failure, especially in patients who have a history of poorly controlled hypertension or diabetes Disorders of Coagulation Disorders of Coagulation Inherited Coagulation Disorders:  Haemophilia A Genetic and present at birth  Haemophilia B (Christmas Disease)  Von Willebrand disease Acquired:  Liver disease – reduced production of coagulation factors  Haemotological malignancy – impaired coagulation  Anticoagulant drugs Haemophilia A Most common type of Haemophilia 1:5000 males aCected DeXciency of clotting factor VIII X-linked recessive condition Males aCected, females are carriers (may also have reduced factor VIII levels) May be mild, moderate or severe The main symptom is bleeding that does not stop oNosebleeds oBleeding gums oSkin that bruises easily oPain and stiCness around joints, such as elbows, because of internal bleeding Haemophilia B (Christmas Disease) ▪ Less common than Haemophilia A ▪ DeXciency in clotting factor IX ▪ X-linked recessive condition ▪ Males aCected, females carriers ▪ 1:5000 males ▪ Same symptoms as Haemophilia A Von Willebrand Disease ▪ Most common hereditary coagulation abnormality ▪ 1% population, male=female ▪ DeXciency or dysfunction of von Willebrand factor (vWF) ▪ vWF function: carrier for factor VIII and mediates platelet adhesion and aggregation Platelets don’t stick together properly and you do not get the platelet plug ▪ Three types: mild, moderate, severe ▪ Presentation similar to platelet dysfunction ▪ Treated with desmopressin, tranexamic acid, factor VIII replacement  Antiplatelet and Anticoagulant Drugs Agents that reduce the ability of blood to form clots or coagulate Exert their affects at different stages of coagulation process Antiplatelets — interfere with platelet aggregation by reversibly or irreversibly inhibiting various steps of platelet activation required for primary haemostasis. Anticoagulants — Inhibit production or activity of the factors required for coagulation cascade - impair secondary haemostasis. Antiplatelet Drugs Indications: Examples: Ischaemic heart disease  Aspirin Previous myocardial infarction  Clopidogrel Atrial Xbrillation  Dipyridamole Coronary stent placement  Ticagrelor Previous stroke  Prasugrel Renal transplant Anticoagulant Drugs Indications: Examples: ▪ Stroke  Warfarin ▪ Transient ischaemic attack  Direct Oral Anticoagulant Drugs ▪ Deep vein thrombosis (DOACs): Rivaroxaban, Apixaban, Edoxaban, Dabigatran ▪ Pulmonary embolism  Injectable Anticoagulant: ▪ Atrial Xbrillation Dalteparin, Enoxaparin, ▪ Heart valve surgery Tinzaparin  Heparin Warfarin  Vitamin K antagonist - blocks one of the enzymes that uses vitamin K to produce clotting factors  Impairs synthesis of factors II, VII, IX, X  Prothrombin time and activated partial thromboplastin time are increased  Monitor by measuring International Normalised Ratio (INR)  Target INR levels diCer depending on the indication for which the drug is prescribed and can range from 2.5-3.5 ± 0.5.  Slowly absorbed and long half-life  ECect begins after 8-12 hours, maximal at 36 hours, persists for 72 hours  Interactions with multiple medications NSAIDs, antibiotics, antifungal Direct Oral Anticoagulant Drugs Rivaroxaban, Apixaban, Edoxaban inhibit factor Xa (10a) coagulation cascade. All reversible inhibitors of factor Xa - prevents thrombin generation and thrombus development Dabigatran direct inhibitor of coagulation factor thrombin. Reversible competitive thrombin inhibitor that directly inhibits the conversion by thrombin of Xbrinogen to Xbrin Direct Oral Anticoagulant Drugs  Rapid onset of action (1-4 hours) in comparison to Warfarin  No need for routine monitoring - cannot measure INR to regulate eCect  Fewer food and drug interactions (antifungals, antibiotics, NSAIDs) so less restrictive and safer than Warfarin  Apixaban, dabigatran, and rivaroxaban have reversal agents  There is currently no reversal agent for edoxaban  Kidney disease or failure having dialysis Heparin ▪ Short half life 1-2 hours ▪ Mainly used IV in hospitals for inpatient care ▪ Also administered subcutaneously ‘Minihep’ reduces risk of deep vein thrombosis in pregnant women, or after surgery ▪ Used to prevent thrombosis after myocardial infarct ▪ Used in IV dialysis to prevent thrombosis in pumps Bleeding risk – get advice before invasive dental treatment Summary Refresh knowledge of haemostasis Classify bleeding disorders Recognise medical conditions and drug therapies that alter bleeding risk Further Reading Dental Update - Special care dentistry: part 3. dental management of pa tients with medical conditions causing acquired bleeding disorders (dent al-update.co.uk) National Institute for Health and Care Excellence (2021). Anticoagulant – oral. Available at: Anticoagulation - oral | Health topics A to Z | CKS | NICE [Accessed 03.10.24] Scottish Dental Clinical ECectiveness Programme (2015). Management of Dental Patients Taking Anticoagulants or Antiplatelet Drugs. Available at: Anticoagulants and Antiplatelets – SDCEP [Accessed 04.10.24] The Haemophilia Society (2021). Bleeding Disorders. Available at: Bleeding Disorders | The Haemophilia Society [Accessed 04.10.24] Waugh A, Grant A (2018). Ross & Wilson Anatomy and Physiology in Health and Illness (13th Ed). Elsevier. References Nizarali, N., & RaXque, S., 2024. Special care dentistry: part 3. Dental management of patients with medical conditions causing acquired bleeding disorders. Dental Update, 40(10), pp.707-709. Cruz-Pamploma, M. et al. 2011. Dental considerations in patients with liver disease. Journal of Clinical and Experimental Dentistry, 3(2), pp.127-135. Available at: http://www.medicinaoral.com/odo/volumenes/v3i2/jcedv3i2p127.pdf [Accessed 04.10.24] National Institute for Health and Care Excellence (2021). Anticoagulant – oral. Available at: Anticoagulation - oral | Health topics A to Z | CKS | NICE [Accessed 03.10.24] Scottish Dental Clinical ECectiveness Programme (2015). Management of Dental Patients Taking Anticoagulants or Antiplatelet Drugs. Available at: Anticoagulants and Antiplatelets – SDCEP [Accessed 31.10.24] The Haemophilia Society (2021). Bleeding Disorders. Available at: Bleeding Disorders | The Haemophilia Society [Accessed 01.11.24]