thrombotic disorders Flashcards
virchows triad - risk factors for thrombosis
vascular injury
- atheroscerlosis
- trauma
- surgical manipulation
- prior thrombosis
stasis
- immobility
- pressure
- increased viscosity
hyper coagulability
- increased procoagulants
- decreased inhibitors
describe deep vein thrombosis and its presentation
thrombosis of left veins
leg swelling, pitting oedema, leg pain
venous discolouration
often clot can break off and cause emboli (PE)
signs and symptoms of pulmonary embolism
symptoms
- chest pain
- SOB
- blood in cough
signs
- tachycardia
- tachypnoea
- hypoxia
testing for PE
D-dimer
CT pulmonary angiogram performed
V/Q scan
define D-dimer
measure the products of fibrin breakdown
- positive in DVT and PE
- also positive with inflammation, surgery etc
define thrombophilia
- tendency to develop thrombosis
- acquired and/or inherited
- manifests as VTE
causes of VTE
1/3 = spontaneous 2/3 = provoked events - surgery, trauma - immobility, hospitalisation - malignancy - HRT, COCP, pregnancy
inherited thrombophilia
abnormal inhibitor function
- resistant to activated protein C
- due to mutant factor V Leiden
deficiency of inhibitors
- antithrombin, protein C and S
increased factor levels
- prothrombin gene mutation
- elevated factor VIII
factor V leiden
normal coagulation factor Va is inactivated by protein C
factor V leiden is the mutation form and as a result can’t be inactivated by protein C so continues
leading to increased risk of venous thrombosis
single point mutation
thrombophilia testing
- measuring factor V leiden and prothrombin gene mutation
- also measure natural inhibitors
more sever
number 1 treatment for VTE
LMWH and warfarin
heparin
- increases antithrombin effect (inhibits thrombin)
- given initially, immediate effect
- prolongs APTT however this can be reversed with protamine
LMWH effect
increases antithrombin effect (inhibits Xa)
subcutaneous with better bioavailability
doesn’t cause significant APTT or TCT prolong
warfarin
- monitor with INR
- interaction with many drugs
- lag between starting drug and effect, due to vitamin K stores
positives and negatives of direct acting oral anticoagulants
positives
- no monitoring required
- fixed dose
- less intracranial haemorrhage (compared to warfarin)
negatives
- kidney excretion
