The document discusses the processes involved in normal haemostasis and thrombosis, explaining how blood is maintained in a fluid state while also forming clots to prevent blood loss. It outlines the Virchow triad, which includes endothelial injury, abnormal blood flow, and hypercoagulability as key factors in thrombosis development. Additionally, it explains the distinction between a thrombus and an embolus, detailing how emboli can lead to conditions such as pulmonary embolism and systemic embolism.

1. THROMBOSIS
&
EMBOLISM

2. Normal Haemostasis
Process of maintaining blood in a fluid, clot-free state in normal vasculature.
Arrest of blood loss from damaged blood vessels.
Is a complex of homeostatic reactions, which result in arrest of bleeding from
damaged blood vessels (hemo = blood, stasis = standing)
Is counter-balanced by reactions, which prevent blood coagulation in
uninjured vessels and maintain the blood in a fluid state.
4 overlapping processes or stages
• Local vasoconstriction
• Formation of a platelet plug
• Formation of a web of fibrin proteins that penetrate and surround
the platelet plug – blood coagulation or clotting
• Clot retraction.

3. Thrombosis
Thrombus
• an aggregation of blood factors primarily platelets & fibrin with
entrapment of cellular elements, frequently causing vascular obstruction
at the point of its formation
Thrombosis
• Formation of a solid or a semisolid mass from the constituents of the
blood within the vascular system within life.

4. Virchow Triad
AETIOLOGY OF THROMBOSIS

5. 1. Endothelial Injury
• Trauma
• Bacteria  toxins by Streptococcus, Staphylococcus, Coryanobacterium
• Virus  Hog cholera virus  thrombosis in spleen
• Parasites  Strongylus vulgaris in anterior mesenteric artery of horse
• Tumours invading endothelium
 Normal endothelium is thrombo-resistant, but when injured the highly
thrombogenic subendothelium is exposed and promotes adhesion of
fibrin and platelets.

6. 2. Abnormal blood flow
• RBC , WBC  Heavier  axial stream
• Platelets  Lighter plasmatic / laminar stream
• When blood flow slows down, platelets being the outermost in the blood
stream, fall out to the periphery and stick to endothelium by virtue of their
adhesive property.
• Cause of slow blood flow  Stasis and turbulence
- chronic venous congestion
- aged and debilitated patients
- vericose vein
- congestive heart failure

7. 3. Hypercoagulability
• Congenital
- Factor V Leiden (a mutated form of human factor V, which causes an increase in
blood clotting (hypercoagulability)
- Congenital thrombophilia  typically caused by a deficiency of natural
anticoagulants (e.g. antithrombin III deficiency, protein C deficinecy, protein S
deficiency)
• Acquired
- Obesity
- Pregnancy
- Cancer
- Hormonal contraceptives (Estrogen)

8. Pathogenesis
• Endothelial injury  platelets adhere to sub-endothelial collagen
• Platelets secretes ADP and thromboxane A2
• Platelets expose phospholipid complex  activates intrinsic
coagulation pathway
• Tissue factor from injured endothelium  activates extrinsic
coagulation pathway
• ADP  reversible primary hemostatic plug ADP, thrombin, TXA2 
irreversible secondary plug
• Fibrin deposition around platelets

10. • An embolus is an abnormal mass of undissolved material which passes in
the blood stream from one part of the circulation to another, impacting in
vessels too small to allow it to pass.
• The actual material which passes along the blood stream is termed an
embolus.
• When it impacts and obstructs the flow of blood, this is known as an
embolism.
• Thus when a thrombus in the leg breaks off, this is an embolus, and when it
impacts in the pulmonary artery it is a pulmonary embolism.
Embolism

11. Pulmonary embolism
Embolus lodges in the lungs (most common from deep vein thrombosis)
Systemic embolism
Brain, lower extremities, intestines, kidneys, spleen (arterial emboli from intracardiac
mural or valvular thrombi, aortic aneurysms, atherosclerotic plaques)

12. Pulmonary thromboembolism
 Cause from venous emboli from deep leg veins
 Common in hospitalised and bed ridden patients
 Large thrombus gets impacted at bifurcation of pulmonary artery-saddle embolus