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Path/CR - Thrombosis/Embolism (i) (PE (3 types (microemboli (large nos of…
Path/CR - Thrombosis/Embolism (i)
Thrombus
= aggregate of coagulated blood (platelets, fibrin, RBCs) occurring in flowing blood (NOT a clot)
adherent to vasc endothelium, but can separate/dislodge, become an embolism + get lodged somewhere else (e.g. DVT, PE)
form in arts, veins, heart + capills - causes, mechanisms of damage + consequences different depending on site
predisposing factors = Virchow's triad
1) endothelial damage
vessels become prothrombotic
normal endothelial cells produce substances that are antithrombotic
prostacyclin prevents platelet aggregation
thrombomodulin inhibits coag
plasminogen activator (plasmin precursor, encourages fibrinolysis)
when damaged instead produce platelet aggregating factor + plasminogen activator inhibitors, + surrounding platelets produce thromboxane (increases aggregation)
mainly occurs in arts
causes
ulcerated plaques in atherosclerosis
vasculitis (usually immune-mediated, due to infection)
dysfunction due to haemodynamic stresses (hypertension or turbulence due to scarred valves)
smoking
2) abnormal blood flow
stasis in veins, turbulence in arts normally
should be laminar
platelets in contact with endothelium. promoting endothelial cell activation
no fresh blood - no dilution of activated clotting factors + slow inflow of clotting factor inhibitors
causes of turbulence
endothelial injury/dysfunction, countercurrents, local pockets of stasis (e.g. atherosclerotic plaques + aneurysms, esp @ sties of bifurcation)
causes of stasis
prolonged immobilisation
heart failure (poor CO)
shock (peripheral veins vasoconstrict)
ext pressure
aneurysms
Eddy currents
3) hypercoagulability
primary due to
mutations (e.g. factor V, prothrombin)
deficiencies (e.g. antithrombin 3, protein C/S)
secondary due to
tissue damage (surgery/fracture/burns)
cancer
DIC
hyperoestrogenic states (pregnancy/oral contraceptives)
polycythaemia (increased cells in blood, increased cell:liquid ratio - increased viscosity)
nephrotic syndrome (loss of protein due to kidney damage)
antiphospholipid syndrome (autoimmune, inhibits protein C + S)
dehydration
can cause ischamia + infarction (necrosis due to inadequate blood supply )
fate of a thrombus
propagation (enlargement)
leads to obstruction
embolisation (dislodgement)
travels to another site
dissolution (degradation)
by the fibrinolytic system
recanalisation/reorganisation
new openings in vessels
PE
mild oedema
dyspnoea
severe acute pleuritic pain (worse on inhalation when lungs expand) - due to pleuritis
haemoptysis
sudden death
mainly from deep veins of lower limb + very rarely from right heart
travels via IVC
medical emergency
3 types
massive/saddle
wedges in pul art + causes instant death
uncommon
intermediate
may/may not cause infarct
lung has dual blood supply (bronchial + pul)
necrosis only occurs in patients with and already compromised circulation (e.g. heart failure or shock)
microemboli
large nos of tiny emboli
often asymptomatic
block pul arterioles
leads to right heart failure
rarely can become a PARADOXICAL EMBOLISM
can pass through interatrial / interventricular defect in septum + become system
Dx
D dimers
non-specific
risk of false +ve
CT
pul angiogram