Hi

1. 1
HEMORRHAGE
&
THROMBOSIS

2. 2
Hemorrhage

The leakage of blood from vessels, most often from the damage
to blood vessels or defective clot formation.
capillary bleeding can occur in chronically congested tissues.
Trauma, atherosclerosis, or inflammatory or neoplastic erosion of a
vessel wall also may lead to hemorrhage, which may be extensive
if the affected vessel is a large vein or artery.
The risk of hemorrhage is increased in a wide variety of clinical
disorders collectively called hemorrhagic diatheses.

3. 3 Causes of Hemorrhage
Localized
Trauma
 Atherosclerosis
Inflammatory or
neoplastic erosion
Enlarged inter endothelial gap
Generalized
Hemophilia
Hypo fibrinogenemia
Thrombocytopenia
Deficiency of Vitamin K

4. 4 Reading Assignment
Normal Hemostasis Page # 101
Robbins Pathalogy 10th
Edition

5. 5
Thrombosis

6. 6 Thrombosis
Thrombosis is a blood clot within blood vessels that limits
the flow of blood.
Hemostasis tends to form blood clot – limit bleeding from
injured vessel
Pathologic counterpart of hemostasis is thrombosis –
solid mass of blood constituents
Thrombosis is related to one or more components of
Virchow triad

7. 7

8. 8 Causes and pathogenesis of thrombosis
The primary abnormalities that lead to intravascular thrombosis are
(1) endothelial injury,
(2) stasis or turbulent blood flow,
(3) hypercoagulability of the blood

9. 9
Endothelial Injury
Endothelial layer protect flowing blood from the thrombogenic effect of
sub-endothelial tissue.
Endothelial cell release some Heparin like antithrombotic factor which
prevent thrmobosis.
Heparin like substances are (thrombomudulin, Tissue plasminogen
activator(t.PA), inhibitor platelets aggregation PGI2)
Heparin like subs accelerate anti-thrombine 3 which inhibit the clotting
factor.
Thrombomudulin convert thrombin into activator of protein C which
have anti thrombotic effect.
Inhibition platelets aggregation include PGI2 and prostacyclin.

10. Endothelial Injury
 Endothelial cell also secrete prothrombolic subs these
are thromboplast, VWF(VON WILLIBRAND FACTOR)
inhibitors of tissue plasminogen.
Tissue plasminogen activator which activate tissue
plasminogen and help fibrinolytic activity which prevent
thrombosis.
When the endothelial surface damage the antithrombotic
property is lost and the sub-endothelial surface expose which
result thrombosis.
clashing occur between antithrombotic and pro-thromobotic
activity.
10

11. 11
Endothelial Injury
Endothelial injury leading to platelet activation, trigger
thrombosis by exposing Von Willebrand factor (a
blood glycoprotein that promotes hemostasis,
specifically, platelet adhesion) and tissue factor
(thromboplastin or CD142) is the protein that activates the blood clotting system.
by shifting the pattern of gene expression in
endothelium to one that is “prothrombotic.”
Persistent activation of thrombin and platelets Secretion
of plasminogen activator inhibitors – limit fibrinolysis
and favor the development of thrombi

12. 12
Endothelial Injury
 This change is sometimes referred to as endothelial activation or
dysfunction and can be produced by diverse exposures, including;
 1. physical injury
2. infectious agents
3. abnormal blood flow
4. inflammatory mediators
5. metabolic abnormalities, such as hypercholesterolemia or
homocystinemia
6. toxins absorbed from cigarette smoke.

13. 13
II. ALTERNATIONS IN NORMAL BLOOD FLOW

 Turbulence causes endothelial injury or dysfunction &
countercurrents that contribute to local pockets of stasis.
 Stasis is a major contributor in the development of venous thrombi.
Stasis and turbulence therefore:
1. Promote endothelial activation, enhancing procoagulant activity and
leukocyte adhesion, in part through flow-induced changes in the
expression of adhesion molecules and pro-inflammatory factors
2. Disrupt laminar flow and bring platelets into contact with the
endothelium
3. Prevent washout and dilution of activated clotting factors by fresh
flowing blood and the inflow of clotting factor inhibitors

14. 14 HYPERCOAGULABILITY
 Hypercoagulability can be defined as any disorder of the blood
that predisposes to thrombosis.
Can be divided into;
 1. primary (genetic)
2. secondary (acquired) disorders

15. 15
Hypercoagulability

16. 16
Hypercoagulability

17. 17 Types of Thrombi
Arterial
1. Anywhere in arterial
bed
Cardiac
Venous
1. Superficial or
thrombophlebitis
2. Deep or
Phlebothrombosis

18. 18
Arterial Thrombosis
 Atherosclerosis is the major cause
 Abnormal blood flow
 Endothelial damage
 Occlusive, dry, easily breakable and pale
 Contain platelets, fibrin and few RBCs
 Large and medium size arteries are mainly affected
 Aorta, carotid (Stroke), coronary arteries (MI), intestinal and limb
arteries

19. 19 Cardiac Thrombosis
 Heart chambers
 Attached to wall, not
occlusive
 Prone to embolise into brain,
kidneys and spleen – rich
blood supply
 Heart valves – endocarditis
 Bacterial or fungal infection
damage valves, forming large
thrombus

20. 20
Venous Thrombosis
Mostly develop in veins of the legs (red)
Contain platelets, fibrin and few RBCs
Typically develop in stasis condition and always
occlusive
It may be superficial or deep:
Superficial/thrombophlebitis:
Saphenous vein, rarely embolise
Painful and cause local congestion, swelling and ulcer

21. 21
Venous Thrombosis
Deep venous thrombosis (DVTs)/Phlebothrombosis
Larger leg veins or above knee joint – femoral,
popliteal and iliac vein respectively
Very prone to embolise
Collateral channels avoid obstruction, thus
asymptomatic until it embolized to lungs
Common predisposing factors include surgery,
pregnancy and immobilization

22. 22 Fate of Thrombus
1. Propagation: Enlargement by additional platelets and fibrin aggregation –
Increasing vascular occlusion
2. Embolization: Dislodgement and transportation of a part or whole thrombus in
vessel
3. Dissolution: Shrinkage by fibrinolytics
4. Organization: Ingrowth of endothelium, smooth muscles and fibroblasts
forming capillary channels along the length of thrombus
5. Recanalization: Conversion of thrombus into a vascularized mass

23. 23 Fate of Thrombus

24. 24
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