Thrombosis Flashcards
normal haemostasis
Well-regulated process that maintains blood in a fluid, clot free state in normal vessels and induces the rapid formation of a localised haemostatic plug at the site of vascular injury
Haemostasis and thrombosis are dependent on what three components
- Vessel wall
- Platelets
- Coagulation cascade
thrombosis
the inappropriate activation of blood clotting in an uninjured vessel/minimally injured vessel leading to the formation of a blood clot (thrombus) within the vascular system, which can obstruct the flow of blood
thrombus
an aggregate of coagulated blood containing platelets, fibrin and entrapped cellular elements.
virchows triad
change in surface - endothelial injury
change in flow - stasis and turbulence
change its constituents - hypercoagulability
where in the endothelial surface does thrombosis commonly occur and why
atheromatous plaques
Injury occurs due to HTN(Hypertension), turbulent
flow, radiation
results from -exposure of stroma, increased platelet adhesion
how does turbulent blood flow cause or influence thrombosis
Disrupted flow brings platelets into contact with
the endothelium
Prevent dilution of activated clotting factors by flowing blood
hypercoagulability
alteration of the coagulation pathways
-> predisposes to thrombosis
heritable hypercoagulability
Factor V leiden, protein c/protein s deficiencies,
prothrombin mutations
examples of Acquired Hypercoagulability
Oral contraceptives, pregnancy, malignancy,
nephrotic syndrome
sites of venous thrombus formation
– most commonly due to stasis in capillaries and heart
sites of arterial thrombus formation
most commonly superimposed on atheroma
capillaries and heart
causes of arterial thrombosis
Atheromatous plaque
Smokers
High cholesterol
causes of venous thrombosis
Blood pressure lower – atheroma does not occur
Most begin at valves – turbulence, stasis, occlusion
Venous return from the legs relies on calf muscle
contraction and relaxation
Any fall in blood pressure (e.g. during surgery) can
precipitate development
risk factors for venous thrombosis
Immobility Smoking Cancer Pregnancy Oestrogen therapy
Clinical effects of a arterial thrombus
Loss of pulse
Pale, cold
Painful
Death & gangrene of the affected limb/site
Clinical effects of a venous thrombus
- 95% occur in leg veins
- Tender
- Swollen
- Reddened
fate of a thrombus
Lysis and resolution Organisation - scar tissue Recanalization Propagation Embolization
Recanalization
– ingrowth of new vessel which eventually
join up to restore blood flow, at least partially
Propagation
enlarges leading to vessel obstruction
Embolization
dislodges, travelling to a different site
embolism
An embolus is a detached intravascular physical mass,
which is carried in the circulation until it reaches a vessel
too small to permit its further passage when occlusion
occurs
embolism that arise from a thrombus
thromboembolism
types of embolism
Fat Air or gas Thrombus Bacteria emboli Amniotic fluid Tumour fragments
pulmonary embolism
Venous thrombi in the leg veins can travel to the lungs
Small emboli may cause no effects
larger emboli in pulmonary embolisms can cause
• Chest pain • Shortness of breath • Infarction • Sudden death o Saddle embolus
systemic embolism
Arise in the arterial system
Arise in the heart or from atheromatous plaques
May travel to various sites and cause
examples of systemic embolism
- Brain – TIA, stroke
- Renal – infarction
- Bowel – ischaemic bowel
- Limbs – ischaemia and gangrene
low blood supply
• Imbalance between perfusion and demand of
oxygenated blood to a tissue
ischaemia
Deficient supply of blood
how is ischaemia characterised
insufficiency of O2
lack of nutrient substrates and inadequate removal of
metabolites (perfusion)
Susceptibility of tissues to ischaemia
Blood supply and collateral circulation – may compensate
for reduced perfusion
tissues with what kind of metabolism rate are highly susceptible ischaemia
Organs with high metabolic rate and aerobic metabolism –
susceptible (heart)
tissues of what kind are lowly susceptible to ischaemia
Supporting tissues (fibrous, bone) – less susceptible
infarction
Area of ischaemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
what embolic events cause infarction
Torsion: testicular/bowel
Extrinsic compression
Traumatic rupture
clinical examples of infarction
Myocardial infarction Cerebrovascular accident (infarct) Pulmonary infarction Bowel infarction Ischaemic necrosis of the extremities
causes of iscaemia
THROMBOSIS
EMBOLUS
Local vasospasm
Extrinsic compression of vessel
macrscopic appearances of infarct
Wedge shaped (occluded vessel at apex
early macrscopic appearances of infarct
• Poorly defined, irregular • Narrow rim of hyperaemia at edge due to inflammation
late signs of macroscopic appearances of infarct on solid organ
few RBC lysed some
haemosiderin pigment.
Pale and sharply
defined
late signs of macroscopic appearances of infarct on spongy organ
Firm and brown
Haemosiderin pigment
Microscopic features of infarcts
first 12 - 18hrs
→Necrotic tissue stimulates inflammatory response at
edge (1-2days)
→Phagocytosis of cellular debris and dead tissue
→Reparative phase with scar formation
exception to microscopic features of infarcts
Brain exception – liquefactive necrosis
examples of vulnerable tissue
‘Watershed’ areas (especially during shock/hypotension)
o Splenic flexure of the colon
o Brain
o Deep myocardium
low flow infarction
Impaired blood flow rather than absolute cessation
susceptibility of infarcts
low flow
vulnerable tissue
