1. Thrombosis and embolism

2. Thrombosis
Gangrene
Infarction
Embolism

3. Thrombosis
inappropriate clot formation within the circulation

4. pathogenesis is given by Virchow’s triad
endothelial injury
stasis or turbulence of blood flow
blood hypercoagulability

6. Endothelial Injury The dominant of the three
Dysfunctional endothelium may elaborate greater amount of pro-coagulant factors or may synthesize lesser amount of anti-coagulant effectors.
Seen commonly in
HTN, trauma, radiotherapy, smoking

7. Hypercoagulability
any alteration of the coagulation pathways that predisposes to thrombosis

8. Hyper-coagulable statesPrimary (Genetic)
Mutations like –
- Fctor V
- Mutation in prothrombin gene
Deficiencies like –
- Antithrombin III deficiency
- Protein C deficiency
- Protein S deficiency   

9. Secondary (Acquired) Prolonged bed rest or immobilization
Atrial fibrillation
Tissue damage (surgery, fracture, burns)
Cancer  
Cardiomyopathy
Hyperestrogenic states (pregnancy)
Oral contraceptive use    
Smoking, Obesity

10. Thrombi can form in
Heart
Arterial tree
Veins

11. Thrombosis within arteries can lead to necrosis of tissues which it supplies
Ex-thrombosis in the coronary vessels lead to myocardial infarction
Thrombosis within the renal artery leads to renal infarction

12. Thrombosis in the viens can cause blockage of venous drainage of tissues
clots formed within leg veins can ascend to block the pulmonary circulation
Pulmonary embolism

13. Fate of a thrombus Propagation Dissolution Embolisation Organisation
Recanalisation

15. Infarction
Area of ischemic necrosis caused by occlusion of either arterial supply or the venous drainage in a particular tissue
99% infarcts are from thrombotic/embolic events and almost all are from arterial occlusion. Eg
Myocardial infarction
stroke
gangrene of limbs due to peripheral vascular disease

16. Factors influencing infarction:
Nature of blood supply
Lungs have dual supply from pulmonary and bronchial arteries
Liver has dual supply from hepatic artery and portal vein
Kidney, spleen and brain have end arteries with no anastomosis
Rate of occlusion: if slow, can allow for collateral formation,
Tissue vulnerability to hypoxia: neural tissue is the most susceptible, dying within 3 to 4 minutes, and myocardium within 30 to 40 min
Oxygen content in the blood: increased risk of infarction in anemic and cyanosed patient

17. Gross Morphology
Infarction starts as a poorly defined wedge shaped area, with exudates and hemorrhagic area, which gets more defined by a rim of inflammation after some days.
2 types according to gross appearance

18. Red infarct due to venous obstruction
Due to infarction of tissues with dual blood supply like intestine
Due to reperfusion-restoring blood supply

20. White infarct
Solid organs like kidney and liver with arterial occlusion

24. Gangrene
Gangrene refers to the death of body tissue due to a lack of blood flow complicated by bacterial infection.
Gangrene most commonly affects the extremities, including toes, fingers and limbs

26. Embolism
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
99% of the emboli are dislodged thrombi, hence, the term THROMBOEMBOLISM
Potential consequence of embolism is INFARCTION of the tissue distal to it.

27. Types Thromboembolism Fat embolism eg after fractures
Air embolism, eg in open carotid injury,after obstetric proceedures.
Amniotic fluid embolism in pregnancy

28. Pulmonary thromboembolism
A common cause of death among hospitalized patients
In greater than 95% of cases, pulmonary emboli originate from deep leg vein thrombi above the level of the knee
Immobilization is a strong risk factor

30. What is fat embolism Describe the patho physiology of the tissue damage in fat embolism

31. Thank you….