Haemostasis Clinical Context

Question 1

What are primary haemostasis defects?

Answer 1

collagen

• age collagen less able to support blood vessels (senile pupura)
• steroid therapy (bruising as blood vessels more fragile and supporting tissue breakdown)
• scurvy (no Vit C to cross link fibrin)

VWF disease (genetic)

platelets

• increase use of aspirin like drugs (NSAIDS - neurofen, voltaroil) that inhibit platelet aggregation
• thrombocytopaenia (lack of platelets)

Question 2

Signs of 1o haemostasis defects?

Answer 2

never start coagulation
immediate, easy bruising
nosebleeds/menorrhagia common/gums/after surgery
PETECHIAE (small bleeding spots on legs in thrombocytopaenia)

Question 3

What are secondary haemostasis defects?

Answer 3

poor thrombin burst leading to poor fibrin mesh so cannot stabilise platelet plug
GENETIC
- haemophilia (factor 8/9 deficiency)
ACQUIRED
- liver disease (coagulation factors made here)
- drugs like warfarin (inhibit coagulation factor synthesis)
- dilutional coagulopathy (volume replacement in sever injury loses CFs)
- consumption/DIC

Question 4

What is DIC?

Answer 4

generalised coagulation activation
TF in vasculature and IL6 stimulates blood and endothelial cells to make TF
in sepsis/major tissue damage/inflammation CFs/platelets/fibrinogen are depleted so widespread bleeding from IV lines, bruising and fibrin deposition leads to organ dysfunction

Question 5

What are the bleeding patterns of 2o defects?

Answer 5

delayed and prolonged
not from small cuts as bleeding stops after 10 mins
bleed after surgery, nosebleeds are rare
deeper bleed in joints and muscle

ECCHYMIOSIS - easy, large bruising
HAEMARTHROSIS - hall mark of haemophilia, painful bleed into joints causing joint damage/arthropathy

Question 6

What are fibrinolysis defects?

Answer 6

excess fibrinolytic (plasmin, tPA) - tumours, therapeutic admission as tPA given from strokes, venous thrombosis

deficient antifibrinolytic (antiplasmin) - genetic

excess anticoagulant (heparin, thrombin, 10a) - therapeutic admission

Question 7

What is an abnormal thrombus?

Answer 7

pathological clot formation not preceded by bleeding in intact vessel
arterial - MI, stroke, limb ischaemia
venous - pain/swelling

embolism is migration of thrombus
arterial - stroke, limb ischaemia
venous - to lungs as pulmonary embolism with SOB, chest pain and sudden death

Question 8

What is the prevalence of venous thromboembolism?

Answer 8

cause of 10% hospital deaths
25k preventable deaths/year
incidence increases with age, doubles per decade and is from 1/1000-10000 per annum
mortality 5%, 20% recurrence after 1st clot
causes thrombophlebitic syndrom (TPS) - painful leg 23%

Question 9

What are the causes of thrombosis?

Answer 9

MULTICAUSAL - genetic and acquired risk factors
genetic
age, meds, illness,
acute stimuli

Question 10

What is Virchows Triad?

Answer 10

3 factors contribute to thrombosis
blood - AT
- deficient anticoagulant proteins e.g. antithrombin, protein C/S (COCP reduced protein S [])
- increased coagulant activity by factor 8/11
- factor 5 Leiden
- thrombocytosis (increase platelets)

vessel wall - VT
- altered/decreased thrombomodulin, TF, increased TFPI expression in inflammation, malignancy, infection, immune disorders

flow - BOTH
- stasis = reduced flow so CFs accumulate from long haul flight, surgery, fracture, bed rest

Question 11

What is factor 5 leiden?

Answer 11

mutated F5 molecules leads to activated protein C resistance
polymorphic, hereditary
white, Caucasians, 5% of people

Question 12

What is thrombophilia?

Answer 12

at increased risk of thrombosis

Question 13

What situation is the biggest thrombosis risk factor?

Answer 13

hospital

• inflammation
• bed rest
• underlying condition

initial weeks after surgery risk of post operative VTE is 100x higher / 15/16x higher daily admission than normal pop

assess all hospital admissions from VTE risk assessment
give prophylactic antithrombotic therapy, heparin for inpatients, TED stockings

Question 14

How to treat blood clots?

Answer 14

lyse clot with tPA (high risk of bleeding)

limit recurrence with anticoagulant therapies

• increase anticoagulant activity with heparin (immediate)
• decrease procoagulant factors (antiplatelets, warfarin - oral and long term because slow acting)
• inhibit procoagulative factors (Rivaroxabin, Apixabin, Dabigatran)

Question 15

What should high risk thrombosis patients receive?

Answer 15

anticoagulant therapy as thromboprophylaxsis