Thrombosis is the formation of a thrombus, a blood clot within the cardiovascular system, which can involve both blood vessel walls and the blood clotting system. It can arise from endothelial injury, abnormal blood flow, or hypercoagulability and is classified based on location, infective agent, and color. The consequences of thrombosis can vary, leading to conditions such as infarction, ischemic necrosis, and in severe cases, sudden death.

2. DEFINITION
 THROMBOSIS is the formation of a clotted mass of
blood within the cardiovascular system.
 The clotted mass is called as THROMBUS.
THROMBUS BLOOD CLOT
1- Involves wall of blood
vessels, formed elements
of blood & blood clotting
system.
1- Involves only blood
clotting system.
2- composed of platelets
and fibrin.
2- composed of fibrin only.
3- may be life-threatening. 3- mostly life saving.

3. THROMBUS – GROSS PATHOLOGY

4. THROMBUS – MICROSCOPIC PATHOLOGY

5. Antithrombotic & prothrombotic
property of endothelial cells

6. AETIOLOGY:-

7. 1- Endothelial injury :-
 Trauma
 Bacteria- Toxins by Erysipelothrix, 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 thromboresistant, but when
injured the highly thrombogenic subendothelium is
exposed and promotes adhesion of fibrin and
platelets.

8. 2- Abnormal bloodflow:-
 RBC , WBC – Heavier axial stream
Platelets – Lighter plasmatic / laminar stream
 When blood flow slows down, platelets beingd the
outermost in the blood stream, fall out to the periphery
and stick to endothelium by virtue of their adhesive
property.
 Cause of slow bloodflow – Stasis and turbulence
1- chronic venous congestion
2- aged and debilitated animals
3- vericose vein- nasal submucosa in cattle, scrotal
plexus of horse, large veins of broad ligament of bovine
uterus
4- congestive heart failure

9. 3- Hypercoagulability :-
 Increase in level of fibrinogen, prothrombin, factor
VIIa, VIIIa, Xa
 Increse in number of platelets
 Decrease in levels of antithrombin III, protein C and
fibrinolysin
Hepatic disease - formation of prothrombin
Bile deficiency in intestine - less absorption of Vit-K

10. Pathogenesis :-
 Endothelial injury – platelets adhere to
subendothelial collagen
 Platelets secretes ADP and thromboxane A2
 Plateles 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

11. Classification :-
(A) According to location-
 1-Cardiac thrombus
Valvular thrombus- in valves – Erysipelothrix infection in
pig
Mural thrombus – in wall of heart – Clostridium infection in
cattle
 2- Arterial thrombus - Strongylus vulgaris in anterior
mesenteric artery of horse
 3- Venous thrombus – more common in human
 4- Capillary thrombus
 5- Lymphatic thrombus

12. VALVULAR THROMBUS MURAL THROMBUS

13.  (B) According to location within the blood vessel :-
 Lateral thrombus – one side of BV
 Occluding thrombus – entire circumference of BV
 Saddle thrombus – at bifurcation of BV
 Canalised thrombus – new blood channels through the clot
 (C) According to infective agent :-
 Septic thrombus – contains bacteria
 Parasitic thrombus – contains parasites
 Aseptic thrombus – no bacteria or parasites
 (D) According to colour :-
 Pale or white thrombus – in rapid blood flow, only platelets
 Red thrombus – in slow blood flow, fibrin attach to platelets
 Mixed thrombus – most common
 Laminated thrombus – alternate layers of white and red

14. WHITE AND RED THROMBI

15. Fate of thrombus :-
 Propagation
 Emboli formation – foreign body
floating in the blood
 Abcessation – when pyogenic
bacteria present
 Dissolution – by fibrinolytic activity
 Organisation and recanalisation
 Calcification

16. Effects:-
 Negligible effect in vessels which are not required or
where sufficient colateral circulation is present or in large
vessels
 Passive congestion and edema – as obstruction in
venous return
 Infarction – Thrombosis in end arteries lead to ischemic
necrosis
 Gangrene of limbs and intestine
 Interference with cardiac function
 Colic
 Lameness
 Septicemia or pyemia
 Sudden death in coronary artery thrombosis

17. Rudolf Virchow