Thrombosis

2. THROMBOSIS
Dr. Afsar Saeed Shaikh
M.B.B.S, M.Phil.
Assistant Professor of Chemical Pathology
Pathology Department, KEMU, Lahore.

3. INTRODUCTION
 NORMAL HEMOSTASIS
1) Maintain blood in fluid form
in normal blood vessels
2) induce a rapid & localized
hemostatic plug formation at the
site of vascular injury
 THROMBOSIS
‘Pathologic opposite to
hemostasis’

4. INTRODUCTION
 DEFINATION:
‘An inappropriate activation of
normal hemostatic processes,
such as the formation of a
blood clot in uninjured
vasculature or thrombotic
occlusion of a vessel after
relatively minor injury.’

5. INTRODUCTION
 ETIOLOGY:
 Endothelial Injury
 Abnormal Blood Flow
 Hypercoagubality

6. Virchow Triad

7. 1. Endothelial Injury
 General:
 A dominant influence
 Can act without combination with
other factors
 Important factor where normally
high flow rates hampers thrombus
formation e.g. arterial circulation &
heart chambers

8. Endothelial Injury
 Sites :
 Within cardiac chamber (e.g.
following M.I)
 Over ulcerative atherosclerotic
plaques
 At the site of inflammatory or
traumatic vascular injury

9. Mechanism of Endothelial
Injury
 1: Direct endothelial injury;
physical loss of endothelium
 2: Dysfunctional endothelium
(Imbalance of anticoagulant and
pro-coagulant properties of
endothelium)
Continued…….

10. Dysfunctional Endothelium
1. Stress of hypertension
2. Bacterial endotoxins
3. Turbulent flow over scarred valves
4. Hypercholesterolemia
5. Products absorbed from cigarette
smoke
6. Irradiation.

11. 1. Abnormal Blood Flow
 Turbulence:
 Arterial & cardiac thrombosis
 A cause of endothelial injury
 Also causes countercurrents and
local pockets of stasis
 Stasis:
 Venous thrombi
 Acts by disturbing normal blood
flow

12. Mechanism of Abnormal Blood
Flow
 Normal blood flow; laminar
 Turbulence & stasis disrupt normal
laminar blood flow
 Bring platelets in contact with
endothelium
 Prevent dilution of clotting factors
 Retard the inflow of inhibitors
 Promote endothelial cell activation

13. Clinical Settings of Abnormal
Blood Flow
 Ulcerative atherosclerotic plaques
 Aortic & arterial aneurysms
 MI
 Mitral valve stenosis
 Hyperviscosity syndrome
 Sickle cell anemia

14. 3. Hypercoagubility
 Important but less frequent
contributor
 ‘Any alteration of the coagulation
pathways that predisposes to
thrombosis’

15. Causes of Hypercoagubality
 PRIMARY (Genetic)
 Common:
Mutation in factor V gene
Mutation in prothrombin gene
 Rare:
Antithrombin III deficiency
Protein C def.
Protein S def.

16. Causes of Hypercoagubality
 Secondary (Acquired)
 High Risk:
Prolonged bed rest
MI, Cancer, DIC
Atrial fibrillation
Tissue damage
Prosthetic cardiac valve
Antiphospholipid antibody syndrome

17. Causes of Hypercoagubality
 Secondary (Acquired)
 Low Risk:
Cardiomyopathy
Nephrotic syndrome
Pregnancy, Oral contraceptives
Sickle cell anemia
Smoking

18. Types of Thrombi
 Types:
 Arterial Thrombi
 Venous Thrombi
 Mural Thrombi
 Red Thrombi (Stasis thrombi)
 White Thrombi (Gray-white)

19. Morphology of Thrombi
 Arterial:
 Usually occlusive
 Firmly attached to the injured artery
wall
 Gray-white and friable
 Composed of a meshwork of
platelets, fibrin, erythrocytes, and
degenerating leukocytes

20. Morphology of Thrombi
 Venous:
 Invariably occlusive
 Not firmly attached to the artery wall
 Red in color and not friable but wet
like a in-vitro clot
 Contain more erythrocytes as
compare to arterial thrombi

21. THANK YOU!

22. Fate of Thrombi
 Propagation
 Embolization
 Dissolution
 Organization and recanalization