THROMBOSIS
THROMBOSIS
THROMBOSIS
It is the formation of a clotted mass of
blood within the cardiovascular system.
The clotted mass is called the Thrombus.
AETIOLOGY
Virchow’s Triad
1. Endothelial injury
2. Abnormal blood flow
3. hypercoagulability
ENDOTHELIAL INJURY
1. Trauma
2.Bacteria- Toxins by Streptococcus, Staphylococcus, Coryanobacteria
3.Virus- Hogcholera virus es are responsible for causing thrombosis in
spleen .
4. Tumors invading endothelium.
Normal endothelium is thromboresistant but when injured the highly
thrombogenic subendothelium is exposed and promotes adhesion of
fibrin and platelets .
ABNORMAL BLOODFLOW
RBC’S , WBC’S are heavier show axial stream
Platelets are lighter and show laminar stream
When blood flow slows down, platelets fall out to
the periphery and stick to endothelium by virtue of
their adhesive nature.
CAUSES OF SLOW BLOODFLOW
1.Stasis
2.Turbulence
HYPERCOAGULABILITY
Increase in level of fibrinogen, prothrombin
Increase in number of patelets
Decrease in levels of antithrombin 3, protein c and
fibrinolysis
Factors responsible for hypercoagulable
state
•1. Primary (hereditary) factors
•Deficiency of antithrombin 3rd
•Deficiency of protein C and S
•Defects in fibrinolysis
•Increased levels of coagulation factors (2nd and 7th)
• Secondary (Acquired ) factors
•Antiphospholipid antibody syndrome
It is a disorder in which the immune system attacks
normal proteins in the blood.
There are two types of APLA
1. Lupus anticoagulant antibody
2. Anti cardiolipin antibody
PATHOGENESIS
Endothelial injury
Low density lipoprotein enters the damaged endothelial wall
WBC’S die and deposit itself under the damaged endothelium
• Foam cells are formed.
• Fatty streak is formed with the deposition of fibrin.
• Platelets start to gather at the damaged endothelium
• Smooth muscle secretes collagen,proteoglycan,elastin fibrous cells that wall around the
fatty streak
• Plaque is formed
• Crystallisation occurs
• Protein build up In the inner wall of arteries
• Blot clot is formed
CLASSIFICATION
•According to location-
•Cardiac thrombus
•Arterial thrombus
•Venous thrombus
•Capillary thrombus
•Lymphatic thrombus
B. According to location within the
blood vessel
Lateral thrombus – on one side of blood vessel
Occluding thrombus- entire circumference of blood
vessel
Saddle thrombus- at bifurcation of blood vessel
Canalised thrombus- new blood channels through
the clot
C. According to infective agent
Septic thrombus – contain bacteria
Parasitic thrombus – contain parasites
Aseptic thrombus - new blood channels through the
clot
D. According to colour
Pale or white thrombus- in rapid blood flow,
characterised by predominance of platelets.
Red thrombus- in slow blood flow, characterised by
predominance of red blood cells.
Mixed thrombus – most common
alternate layers of white and red
FATE OF THROMBUS
Resolution : thrombus resolves
Organisation
1. phagocytosis of fibrin and cell debris
2. Capillary grow into the thrombus
Leukocytes and endothelial cells start digesting coagulum
Propagation: cause obstruction in vessels
thromboembolism
PREVENTION
1. Everyday living
Exercise regularly
Eating a low fat , high fiber diet
Check bp once a year
Drink plenty of fluids
2. After surgery
Anticoagulants (Heparin, Warfarin)
When travelling
Stretch legs
Flex feet
Do ankle pump exercise
TREATMENT
•Warfarin and vitamin K antagonists can be taken orally
•For more effectiveness heparin can be given by IV
injection
•Streptokinase can be administered INRAVENOUSLY
•Ultrasound accelerated thrombolysis can also be given