Thrombosis-Thrombogenesis-Thrombus Morphology- Fate-Clinical Features

TOPICS Covered.

• Thrombosis
• mechanism of thrombus formation
• Types Of Thrombus
• Difference between venous thrombi and postmortem clots
• Fate of Thrombi
• Clinical manifestations and treatment

Thrombosis:
                   It refers to the process of formation of a blood clot in the non-interrupted cardio-vascular system. The main difference between thrombus and embolus is that thrombus remains attached to the vessel wall

Thrombus:
               It refers to the clotted mass of blood in uninterrupted vessels, attached to the vessel wall

Mechanism Of Thrombogenesis

Thrombogenesis means Formation of thrombus.
Mechanism and factors that predispose to thrombogenesis are:

• Endothelial injury
• Statis and turbulence 
• Hypercoagulability
• Autoimmunity

A) Endothelial Injury.
                              Endothelial injury is an obvious cause of thrombus formation. but is important to note that there is an only endothelial injury the whole wall of the vessel is not interrupted. Following events are involved.
1. Exposure of subendothelial collagen to platelets.
2. Activation of the intrinsic pathway of the coagulation system due to contact of factor XII with subendothelial
    collagen.
3. Activation of the extrinsic pathway of the coagulation system due to the release of tissue factor.
4. Local loss of Prostacyclin and plasminogen activator.

Causes Of Endothelial Injury.

Following factors cause endothelial injury

1. Trauma or injury to the blood vessels
2. Inflammatory injury to the vessels
3. Bacterial toxins and endotoxins
4. Stress of hypertension
5. Hypercholesterolemia 
6. Myocardial infarction
7. Myocarditis
8. Homocystinuria
9. Products absorbed from cigarette smoke

B) Stasis and Turbulence:

                                    Stasis and turbulence normally occur in the pockets of blood vessels that normally lies behind the cusps of vessel valves.

Stasis and turbulence cause thrombosis by the following effects.

1. Disruption of laminar flow that allows the platelets to come in contact with the endothelium
2. Prevention of dilution of activated clotting factors to subcritical concentration.
3. Retardation of inflow of clotting factor inhibitors
4. Allowing build up of platelet aggregates and nascent fibrin in the sluggish stream or in pockets of stasis.
5. Promotion of endothelial cell hypoxia Therefore it promotes aggravate the endothelial injury

Site Of Stasis and Turbulence:

1. Sinuses behind the valve cusps in deep veins of the lower leg
2. Auricular appendages of heat when there is atrial fibrillation or massive dilation of atria as in mitral stenosis
3. Aneurismal dilatations.

C) Hypercoagulability.

                                    Hypercoagulability refers to the alteration of the blood clotting mechanism that predisposes to Thrombosis

Causes of hypercoagulability

1. Oral contraceptives
2. Following trauma or surgery
3. Following severe burns
4. Advanced Age, bed rest and immobilization
5. In the later pregnancy or postpartum state
6. Nephrotic syndrome
7. Hereditary lack of natural anticoagulants
8. Disseminated Cancer

Oral contraceptives increase the concentrations of fibrinogen, prothrombin and factors VII, VIII, and X in the plasma

In disseminated cancer, hypercoagulability is due to secretion of thrombogenic factors by tumour necrotic cells.

In trauma, hypercoagulability is due to vascular injury.

D) Autoimmunity:

                         Autoimmune reactions are involved in vascular injury and cause thrombus formation. for example, Auto-antibodies directed against anionic phospholipids cause thrombosis in SLE by

1. Induction of platelet aggregation
2. Inhibition of prostacyclin production by endothelial cells
3. Interference in the generation of protein C.

TOPICS.

• Thrombosis
• mechanism of thrombus formation
• Types Of Thrombus
• Difference between venous thrombi and postmortem clots
• Fate of Thrombi
• Clinical manifestations and treatment