20. Thrombosis/Embolism Flashcards
Definition of thrombus
aggregate of coagulated blood containing platelets, fibrin, and RBC that occurs in FLOWING blood
- diff from a clot
- adhere to endothelium but can separate
Clinical consequence of separation of a thrombus from vessel
Becomes an embolus
Thrombus aetiology
Virchow’s triad
- endothelial damage
- abnormal blood flow
- hypercoagulability
What happens during endothelial damage
Normal endothelial cells profuces substances that
- reduce thrombi formation
- prevent platelet aggregation
- inhibit coagulation
- encourage fibrinolysis
Substances that normal endothelial cells produce in a prothrombotic state
- prostacyclin - platelet inhibitor
- thrombomodulin - antithrombin
- plasminogen activator - degrades fibrin clots
- nitric oxide
Substances that damaged endothelial cells produce in a prothrombotic state
- platelet aggregating factor
- plasminogen activator inhibitors
- platelets produce thromboxane which causes further platelet aggregation
Causes of endothelial damage in arteries
- ulcerated plaques in atherosclerotic arteries
- vasculitis
- endothelial dysfunction due to haemodynamic stresses of hypertension or turbulent flow over scarred valves
- cigarette smoke
Effects of abnormal blood flow
- disrupts laminar flow and brings platelets into contact with the endothelium
- prevents dilution of activated clotting factors by fresh flowing blood
- slows inflow of clotting factor inhibitor and permits the build up of thrombi
- promotes endothelial cell activation
What cayses turbulence in arteries and heart
- endothelial injury or dysfunction
- countercurrents and local pockets of stasis
- ulcerated atherosclerotic plaques
- aneurysms
- sites of arterial bifurcation
What causes stasis venous thrombi
General -prolonged immobilization in bed -heart failure -shock Local -external pressure -aneurysm -eddy currents
Primary disorders that increase coagulability
primary = genetic
- mutation in factor V gene (factor V Leiden)
- mutation in prothrombin gene
- antithrombin III deficiency
- Protein C and S deficiency
Secondary disorders (more common) that increase coagulability
secondary = acquired
- tissue damage (surgery, fracture, burns)
- cancer
- DIC
- APS
- OCP
- hyperestrogenic state (pregancy)
- nephrotic syndrome
- polycythaemia
What are the clinical consequences of
a) arterial thrombi
b) venous thrombi
a) ischaemia/infarction and emboli into other arteries/arterioles
b) emboli into venous side of circulation
- e.g. pulmonary arteries -> lungs -> infarction
Causes of thrombosis in
a) arteries
b) veins
a) atherosclerotic plaques, turbulence, stasis, hypertension, counter currents
b) stasis, hypercoagulability
What happens to a thrombus
- propagation
- thrombus enlarges, leading to vessel obstruction - embolisation
- thrombus dislodges, travelling to a different site - dissolution
- thrombus degraded by fibrinolytic system - organisation and recanalisation of blood vessels
Clinical effects of arterial thrombosis
- infarction
- cell necrosis due to reduced blood supply with thrombus at site
- e.g. MI, cerebral infarction, acute limb ischaemia - embolise peripherally through arteries
- infarcts brain, kidneys, spleem
Difference between thrombus and embolus
Thrombosis occurs when a thrombus, or blood clot, develops in a blood vessel and reduces the flow of blood through the vessel.
Embolism occurs when a piece of a blood clot, foreign object, or other bodily substance becomes stuck in a blood vessel and largely obstructs the flow of blood.
Effects of venous thrombosis
- Localised
- may be asymptomatic
- oedema, pain
- may cause necrosis and gangrene - Distant
- PE
- venous sinuses of the skull secondary to infection of the middle ear, mastoid or paranasal sinuses (less common)
Causes of thrombosis in capillaries
- frost bites
- burns
- haemolytic anaemia such as sickle cell disease or autoimmune disease with cold agglutinins
Effects of thrombosis in capillaries
necrosis and ulceration
Thrombosis in the heart
- mural thrombus post MI
- thrombotic vegetations on cardiac valves in infective endocarditis
- thrombosis in left atrium, esp auricular appendix in atrial fibrillation
What is embolism
an embolus is a detached intravascular physical mass that arises from one part of the circulation and travels to another part of the circulation
- can be systemic or pulmonary
- can be solid, liquid or gas
Characteristics of pulmonary embolism
- arises mainly in the deep veins of the lower limbs, but occasionally can arise in the right side of the heart
- carried in circulation along the IVC through the right side of the heart and gets caught in the lung circulation
Types of pulmonary emboli
- massive
- wedges in the pulmonary artery
- resulting in sudden death
- Saddle embolus - straddles the bifurcation of the pulmonary trunk extending to the left and right pulmonary arteries - intermediate
- may or may not cause infarction
- lungs have dual blood supply (bronchial + pulmonary)
- necrosis only occurs in patients whose circulation is already compromised (heart failure/shock) - microemboli
- large numbers of tiny emboli gets into the circulation
- blocks small pulmonary arterioles -> right heart failure
What are the cause of air/gas embolism
- damage to the veins of head and neck
- during inspiration, the negative pressure from the thorax is transmitted to the head and neck vein
- damaged/cut veins causes air to be sucked in during inspiration
- blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system
