Thrombotic Disorders Flashcards
Tissue Plasminogen Activators
Promotes Plasminogen to plasmin which results in the breakdown of fibrin to fibrinogen
Thromboembolism
Movement of clots along a vessel to other parts of the body
Virchows Triad
Stasis, Hypercoagulability, Vessel Damage
Arterial Thrombus
Formation of white clots - platelets and fibrin. This results in ischaemia and infarction. Usually second to athersclerosis
Risk Factors for Arterial Thrombosis
Age Smoking Sedentary lifestyle Hypertension Diabetes mellitus Obesity Hypercholesterolaemia
Management of Arterial Thrombosis
Primary prevention
Lifestyle modification
Treatment of vascular risk factors
Acute presentation
Thrombolysis
Antiplatelet/anticoagulant drugs
Venous thrombosis
Fibrin and red cell accumulation. This results in back pressure. Principally due to stasis and hyper-coagulability.
Types of Venous Thromboembolism
Limb deep vein thrombosis Pulmonary embolism visceral venous thrombosis (portal vein) intracranial venous thrombosis superficial thrombophlebitis
Risk factors for venous thrombosis
Increasing age Pregnancy Hormonal therapy (COCP/HRT) Tissue trauma Immobility (plaster cast immobilisation after a fracture or lengthy hospital inpatient stay) Surgery Obesity Systemic Disease Family History (specific to first degree relatives)
Systemic Disease increasing risk of venous thrombosis
Cancer
Myeloproliferative Neoplasm
Autoimmune IBD, connective tissue disease, antiphospholiid syndrome
Diagnosis of Venous Thrombosis
Pretest probability scoring (Wells Score, Geneva Score)
Laboratory testing if pretest probability low (D-dimer)
Imaging (Doppler US, then move onto contrast venography, CT venography or MRA)
Imaging for PE
Ventilation/Perfusion Scan (V/Q) or CT pulmonary angiogram
Aims of management of venous thromboembolism
Prevent clot extension
Prevent clot embolisation
Prevent clot recurrence in long term treatment
Management of VTE
Anticoagulants
- LMWH (block anti-tna)
- Coumarins (warfarin) which is a vitamin K antagonist and reduced the circulating volume of vitamin K dependent coagulation factors
- DOACs (rivaroxiban etc)
Thrombolysis in selected case
-in a massive PE
Heritable Thrombophilia
an inherited predisposition to venous thrombosis. Mostly due to Factor V Leiden mutation. Va becomes resistant to its breakdown (activated protein C resistance)
Microvascular Thrombosis
Affects extremities. Marked ischaemia in the peripherys. Can be platelet and or fibrin clots.
Diffuse Intravasular Coagulation occurs in
Septicaemia
Malignancy
eclampsia
Presentation of DIC
Gangrene and organ failure
DIC
Activation of coagulation cascade and massive increase in clotting and thrombus formation. There is then a reduction in clotting factors and platelets which can result in catastrophic bleeding. Treat with low dose anticoagulant.
Management of the bleeding type of DIC
support with platelets or clotting factors (fresh frozen plasma)
