Haemostasis and bleeding disorders Flashcards
What are the mechanisms of haemostasis called
Primary and Secondary acting simultaneously
Third stage of fibrinolysis also called tertiary haemostasis
What components interact in haemostasis
Complex interaction of blood vessels, platelets, Von Willebrand factor (vWF) and clotting factors
What are the 2 main responses to vessel injury in primary haemostasis
Vascular response = reflex vasoconstriction
Platelet plug formation via vWF
What components are associated with primary haemostasis
Blood vessels
Platelets
Von Willebrand Factor (vWF)
Where are most clotting factors manufactured
Liver
What clotting factors are produced by the endothelial cells of the blood vessels
Factor VIII
vWF
What clotting factors are vitamin K dependent factors
Factor II
Factor VII
Factor IX
Factor X
AY BAWS CAN I HABE DE NOTE PLZ
Clotting factors are present in the circulation in the inactive form
When is tissue factor released and what does it do
Tissue factor released on injury to blood vessel activates the extrinsic pathway
What activates the intrinsic pathway of secondary haemostasis
Exposure to collagen activates the intrinsic pathway
What types of haemostatic disorders can you develop from primary haemostasis
Vascular disorders
Von Willebrand disease
Platelet Disorders
What types of haemostatic disorders can you develop from secondary haemostasis
Clotting factor disorders
What congenital haemostatic disorders can you get
- Von willebrand disease (1/2)
- Haemophilia A (2)
- Haemophilia B (2)
What acquired haemostatic disorders can you get
- Thrombocytopenia (1)
- Platelet dysfunction associated with drugs (1)
- Antiplatelet therapy (1)
- Anticoagulant therapy (2)
What does von willebrand factor do
- Mediates platelet adhesion to damaged endothelium
- Mediates platelet aggregation (sticking together) - Stabilises and transport factor VIII
What is vWF disease caused by
vWF deficiency
What are the clinical features of vWF disease
- Can present as problems of either 1 or 2 haemostasis or both
- Bruising, epistaxis
- Prolonged bleeding during surgical and dental procedures common
- GI bleeding and menorrhagia also frequent
What can be done to manage vWF disease
- Desmopressin (DDAAVP) - stimulates release of vWF and factor VIII - Rx of mild form
- vWF replacement using human plasma, rich in vWF and factor VIII- Rx of severe form
- Anti-fibrinolytic drugs to help slow/prevent clot breakdown- given oral or inject
What is the dental relevance of vWF disease
- Prolonged oozing post extraction and bleeding into muscles/joints
- Haematological cover before any invasive procedure in severe cases
- Avoid regional LA (Infiltration or intra-ligamentary safer)
- Avoid aspirin/NSAIDs (acetaminophen or co-codamol safer)
What should be used instead of regional LA for patients with vWF disease
Infiltration or intra-ligamentary LA
What should be used instead of aspirin/NSAIDs for patients with vWF disease
Acetaminophen or co-codamol
Name a hereditary platelet deficiency disorder
Bernard-Soulier syndrome
What mechanisms can cause platelet deficiency disorders
Megakarocyte suppression
Bone marrow failure
Splenomegaly
Increased destruction of platelets
What can cause megakarocyte suppression
- Chemotherapeutic agent
- Viruses - parvovirus infection, mumps, HIV
What can cause bone marrow failure
- Aplastic anaemia
- Leukaemia
- Lymphoma
- Metastases
How can splenomegaly cause platelet deficiency
Causes sequestration of platelets
What can cause the increased destruction of platelets
- Autoimmune - idiopathic thrombocytopenic purpura
- Drugs - cytotoxic drugs
- Diseases - disseminated intravascular coagulation (DIC), SLE, Malaria
What can cause platelet dysfunction disorders
Antiplatelet drugs -
- Aspirin
- NSAIDs
- Clopidogrel, Prasugrel
- Dipyridamole
- vWF disease
Which of the anti platelet drugs has a reversible effect
NSAIDs only
What are the clinical features of platelet disorders
Easy bruising and bleeding
- Petechiae
- Purpura
- Ecchymosis
What is the dental relevancy of platelet deficiency
- Patients with suspected thrombocytopenia - Investigate platelet count (PC) by requesting full blood count (FBC) prior to dental treatment
- Refer to GP/haematologist for further management
- Risk of spontaneous bleeding, PC ˂ 20,000/mm3
What is the dental relevancy of platelet dysfunction
- Minor dental procedures- continue medications
• Treat without interrupting antiplatelet medication
• Never stop medications without consulting their GP
• Limit initial treatment area e.g. single extraction at a time
What hereditary 2 haemostatic disorders are there
- Haemophilia A and B
- vWF
What acquired causes can cause 2 haemostatic disorders
Anticoagulant therapy -
- Warfarin therapy
- Heparin therapy
- Novel/Non-vitamin K oral anticoagulant therapy
What diseases can cause 2 haemostatic disorders
- Liver disease, including obstructive jaundice
- DIC
- Malabsorption syndromes
What causes haemophilia A and B and what chromosome is it found in
- Deficiency factor VIII and IX respectively
- X-linked disorders- affecting ~ 1 in 5000 males
- Females are carriers
How is haemophilia A and B categorised
Based on Factor VIII or IX levels
- Very mild > 25%
- Mild - 5-25% of normal
- Moderate - 1-5% of normal
- Severe - <1%
How can haemophilia be treated
- Desmopressin = increased production of factor VIII
- Replacement therapy for specific clotting factors
- Inhibit fibrinolysis- antifibrinolytic agents
Name some replacement therapies for specific clotting factors
- Clotting factor concentrate from plasma
- Commercially produced recombinant factor
Name some antifibrinolytic agents
Tranexamic acid
Epsilon amino caproic acid
What are the dental aspects of haemophilia
- All preventative - minimise surgical intervention
- Close cooperation with haematologist/specialist dentist
- Big risk of haemorrhage after surgery or injection
- Post operative - watch for hematoma formation
- Trauma to head and neck - prophylactic factor VIII replacement is essential
What are the common indications of thrombosis or risk of thrombosis
- Atrial Fibrillation
- Cardiac Valvular disease
- Mechanical prosthetic heart valves
- Ischaemic heart disease - recent MI
- DVT
- Pulmonary embolism
- Renal dialysis
How is warfarin taken and what does it inhibit
Orally
Inhibits vitamin K dependent factors - II, VII, IX, X
How is warfarin effect reversed and monitored
Monitored = INR/prothrombin time
Reversed with parenteral fresh frozen plasma/vitamin K
AY BAWS CAN I HABE DE NOTE PLZ
Warfarin has narrow therapeutic range & frequent monitoring and dose
adjustment.
Also sensitive to drug interactions.
What dental aspects are present with a patient on warfarin
- Preventive dentistry-minimise surgical intervention
- Dental care - close cooperation with specialist/physician
- Measure INR within 24 hours of surgery
- INR>4 refer for hospital for dental care
What are some of the potential drug interactions that warfarin may have
- Warfarin + metronidazole
- Warfarin + macrolides (erythromycin)
- Warfarin + azole antifungals (miconazole)
- Warfarin + Aspirin/NSAIDs
What are the effects of warfarin interacting with other drugs and how can you minimise the risk of these interactions
- Increased risk of significant bleeding (increases INR)
- Avoid concurrent use of both medications
- Alternative antifungals (Nystatin)
What does heparin inhibit and how long does it last
Clotting factors II and X
Short lived anticoagulant effect
What is used to monitor heparin effect
Activated partial thromboplastin time
What makes heparins good for immediate management of acute thromboembolic events
Short lifespan and rapid onset
What are low molecular weight heparins used for
non-hospitalised ambulatory patients
Name some non vitamin K oral anticoagulants and what factors they inhibit
- Dabigatran- inhibits factor IIa
- Apixaban – inhibits factor Xa
- Edoxaban - inhibits factor Xa
- Rivaroxaban- inhibits factor Xa
What are the advantages of using non vitamin K oral anticoagulants (i think compared to heparins)
- More predictable levels of anticoagulation
- Do not require routine monitoring
- Wider therapeutic range & easier to manage
- More effective and safer
Describe the onset and short life of non vitamin K oral anticoagulants
Rapid onset of action and relatively short half lives allows for rapid modification of patients coagulation
How should you handle a patients NOACS medication if they have a low and high risk of bleeding
Low risk = treat without interrupting
High risk =
Rivaroxaban - if morning dose, delay and take 4 hrs after haemostasis, if evening dose take as normal
Apixaban, dabigatran - miss morning dose, take evening dose as normal
What are the key haemostatic investigations and what each tests for
- Full blood count - platelet count
- Bleeding time - platelet defects
- Prothrombin time (PT)/ international normalised ratio (INR) - extrinsic pathway and warfarin therapy
- Activated partial thromboplastin time (aPTT) - Intrinsic pathway (30-40secs) and heparin therapy
What is the ideal INR and PR
- PT- (10-12 secs)
- INR- universal test (Patient’s PT/Control PT) (0.9-1.2)
What is the expected INR for patients on warfarin
- INR therapeutic range for patients on warfarin (2-3)
What is the expected aPTT for patients on heparin
- aPTT therapeutic range for patients on heparin (1.5-2.5)
What steps should be taken when dealing with patients with bleeding disorders
- Obtains a comprehensive medical history
- Perform a thorough clinical examination
- Request appropriate special investigations
- Consult with haematologist and/or physician
- Refer where necessary to hospital for dental care
