14 - Haemostasis 2 Flashcards
What is haemostasis?
a state of equilibrium between fibrinolytic factors and anticoagulant proteins, and coagulation factors and platelets
What are the characteristics of abnormal bleeding?
- spontaneous
- out of proportion to trauma/injury
- unduly prolonged
- restarts after appearing to stop
What are the symptoms of primary haemostasis disorders?
- prolonged bleeding
- easily bruised
- prolonged epistasis
- prolonged menorrhagia
- get petechiae with thrombocytopenia
What is petechiae?
- typical of thrombocytopenia
- small pin-prick type bleeding spots (more distal on legs)
- appear spontaneously
- not found with VWD
What are the 3 types of von willebrand disease and their characteristics?
- type 1: not enough vWF produced
- type 2: uncorrect vWF produced
- type 3: no vWF produced
What are the 3 defects of primary haemostasis?
- collagen (vessel wall)
- von willebrand factor
- platelets
What are the features of a collagen defect in primary haemostasis?
- due to steroid therapy, age and scurvy
- less able to support blood vessels as get older
- vitamin c required to cross-link fibrin for security
- steroid therapy makes blood vessels more fragile and breaks down supporting tissue
What are the features of a platelet defect in primary haemostasis?
- due to aspirin and thrombocytopenia
- aspirin inhibits platelet activity
- receptors on platelets can be missing
- thrombocytopenia is when there aren’t enough platelets
What are the features of haemophilia?
- haemophilia a: lack of FVIII
- haemophilia b: lack of FIX
- genetic/hereditary
- no thrombin generated so no fibrin produced
- can form primary haemostatic plug
- plug not stabilised so bleeding continues
What are some defects of secondary haemostasis?
- deficiency or defects of coagulation factors
- poor thrombin burst
- poor fibrin mesh
- genetic or acquired
What are the acquired causes of secondary haemostasis?
- liver disease: less liver synthesis so less coagulation factors produced
- drugs: heparin and warfarin cause too much bleeding
- dilution: lower conc. of coagulation factors
- consumption
- disseminated intravascular coagulopathy: excessive activation of clotting cascade leads to depletion of coagulation factors and fibrinogen
What are some genetic causes of secondary haemostasis?
- haemophilia
- antithrombin or protein s/c deficiency
- factor V leiden
What is Virchow’s Triad and its features?
- vessel wall injury: increases thrombus risk with pro-coagulant haemostatic disorder, more likely to be arterial thrombus
- hypercoagulability: more likely to be venous thrombus
- stasis
What is a thrombosis dependent on?
- speed of flow (stasis)
- blood composition (hypercoagulability)
- endothelium integrity (vessel wall injury)
What are the features of thrombophilia?
- increases risk/tendency to form thrombosis
- occurs at young age
- treated with anti-coagulants
What is the treatment and prevention of thrombosis?
- treatment to lyse clots (fibrinolytics and tPA)
- treatment to limit recurrence/extension/emboli:
- heparin: increases anticoagulant activity
- warfarin: lowers procoagulant factors
- rivaroaxaban, apixaban and dabigatran: inhibit
procoagulant factors
- prophylactic antithrombotic therapy
What is the bleeding pattern of secondary haemostasis?
- delayed after primary haemostasis
- prolonged
- deeper (in joints and muscles)
- not from small cuts
- nosebleeds are rare
- bleeding after trauma/surgery
- after injections
- bleeding stops and starts
What is a thrombosis?
- blood clot occurring where its not needed (intravascularly)
- intact blood vessel with clot in it
- venous or arterial (arterial driven by damage to vessel wall)
What is the prevalence of venous thromboembolism?
- 1 in 1000-10000 per annum
- incidence doubles with each decade
- cause of 10% of hospital deaths
What are the consequences of a thromboembolism?
- death
- recurrence
- thrombophlebitic syndrome
- pulmonary hypertension
What are the effects of a thrombosis?
- obstructed blood flow (in artery causes MI, stroke and ischaemia and in vein causes pain and swelling)
- embolism - migration of thrombus (venous to lungs and arterial from heart)
What are the effects of fibrinolysis?
- for vessel repair and dissolution of clot
- cell migration/proliferation
- restores vessel integrity
- defect of clot stability
- excess fibrinolytic (plasmin/tPA) - therapeutic administration and some tumours
- antiplasmin deficiency
What is disseminated intravascular coagulation?
- generalised activation of coagulation (TF overdrive)
- associated with sepsis, inflammation and major tissue damage
- consumes and depletes coagulation factors and platelets
- activation of fibrinolysis depletes fibrinogen stores
- causes widespread bleeding and deposition of fibrin in vessel (causes organ failure)
