14 - Haemostasis 2 Flashcards

1
Q

What is haemostasis?

A

a state of equilibrium between fibrinolytic factors and anticoagulant proteins, and coagulation factors and platelets

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2
Q

What are the characteristics of abnormal bleeding?

A
  • spontaneous
  • out of proportion to trauma/injury
  • unduly prolonged
  • restarts after appearing to stop
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3
Q

What are the symptoms of primary haemostasis disorders?

A
  • prolonged bleeding
  • easily bruised
  • prolonged epistasis
  • prolonged menorrhagia
  • get petechiae with thrombocytopenia
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4
Q

What is petechiae?

A
  • typical of thrombocytopenia
  • small pin-prick type bleeding spots (more distal on legs)
  • appear spontaneously
  • not found with VWD
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5
Q

What are the 3 types of von willebrand disease and their characteristics?

A
  • type 1: not enough vWF produced
  • type 2: uncorrect vWF produced
  • type 3: no vWF produced
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6
Q

What are the 3 defects of primary haemostasis?

A
  • collagen (vessel wall)
  • von willebrand factor
  • platelets
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7
Q

What are the features of a collagen defect in primary haemostasis?

A
  • 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
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8
Q

What are the features of a platelet defect in primary haemostasis?

A
  • due to aspirin and thrombocytopenia
  • aspirin inhibits platelet activity
  • receptors on platelets can be missing
  • thrombocytopenia is when there aren’t enough platelets
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9
Q

What are the features of haemophilia?

A
  • 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
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10
Q

What are some defects of secondary haemostasis?

A
  • deficiency or defects of coagulation factors
  • poor thrombin burst
  • poor fibrin mesh
  • genetic or acquired
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11
Q

What are the acquired causes of secondary haemostasis?

A
  • 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
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12
Q

What are some genetic causes of secondary haemostasis?

A
  • haemophilia
  • antithrombin or protein s/c deficiency
  • factor V leiden
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13
Q

What is Virchow’s Triad and its features?

A
  • 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
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14
Q

What is a thrombosis dependent on?

A
  • speed of flow (stasis)
  • blood composition (hypercoagulability)
  • endothelium integrity (vessel wall injury)
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15
Q

What are the features of thrombophilia?

A
  • increases risk/tendency to form thrombosis
  • occurs at young age
  • treated with anti-coagulants
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16
Q

What is the treatment and prevention of thrombosis?

A
  • 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
17
Q

What is the bleeding pattern of secondary haemostasis?

A
  • 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
18
Q

What is a thrombosis?

A
  • 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)
19
Q

What is the prevalence of venous thromboembolism?

A
  • 1 in 1000-10000 per annum
  • incidence doubles with each decade
  • cause of 10% of hospital deaths
20
Q

What are the consequences of a thromboembolism?

A
  • death
  • recurrence
  • thrombophlebitic syndrome
  • pulmonary hypertension
21
Q

What are the effects of a thrombosis?

A
  • 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)
22
Q

What are the effects of fibrinolysis?

A
  • 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
23
Q

What is disseminated intravascular coagulation?

A
  • 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)