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Venous Thromboembolism-1

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Title: Venous Thromboembolism-1


1
Venous Thromboembolism-1
Dr. Abdelaty Shawky Mohamed Assistant professor
of pathology
2
Topics
  • 1. Pathophysiology of VTE.
  • 2. Clinical presentation of VTE.
  • 3. Investigations of VTE.

3
1. Pathophysiology of VTE
4
Hemostasis and Thrombosis
  • Hemostasis is the physiologic process that
    maintains the blood in a fluid state in normal
    vessels and to induce a rapid and localized
    hemostatic plug at a site of vascular injury to
    stop bleeding.

5
  • Thrombosis is the pathologic process opposite to
    hemostasis it can be considered an inappropriate
    activation of normal hemostatic processes,
    resulting in the formation of a (thrombus) in
    uninjured vessel or after minor injury.

6
  • Both hemostasis and thrombosis are regulated by
    three general components.
  • 1. The vascular endothelium.
  • 2. Platelets.
  • 3. The coagulation cascade.

7
  • Q. What is the role of endothelial cells in
    hemostasis and thrombosis?

8
  • Endothelial cells have both antithrombotic
    activities preventing thrombosis in normal blood
    vessel and also have prothrombotic activities
    favoring thrombosis in injured blood vessels.
  • The balance between endothelial antithrombotic
    and prothrombotic activities critically
    determines whether thrombus formation,
    propagation, or dissolution occurs

9
Antithrombotic Properties
  • Antiplatelet effects by secretion of
    prostacyclin (PGI2) and nitric oxide. Both
    mediators are potent vasodilators and inhibitors
    of platelet aggregation.
  • Anticoagulant effects These effects are mediated
    by
  • a. Thrombomodulin receptors for (thrombin) to
    block its action and also to activate protein C
    which in turn inactivate factors V and VIII.
  • b. Heparin-like molecules receptors for
    anti-thrombin III to block factors IX and X.
  • c. Release of tissue factor inhibitor. These
    inhibit the coagulation pathway.

10
  • Fibrinolytic effects Endothelial cells
    synthesize tissue-type plasminogen activator
    (t-PA), promoting fibrinolytic activity to clear
    fibrin deposits from endothelial surfaces .

11
Prothrombotic Properties
  • Platelet effects
  • - Endothelial injury leads to adhesion of
    platelets to the underlying extracellular matrix
    this is facilitated by endothelial production of
    von Willebrand factor (vWF), an essential
    cofactor for platelet binding to subendothelial
    collagen.

12
  • Procoagulant effects Endothelial cells
    synthesize tissue factor, which activates the
    extrinsic clotting cascade.
  • Antifibrinolytic effects Endothelial cells also
    secrete inhibitors of plasminogen activator
    (PAIs), which inhibits fibrinolysis.

13
Coagulation cascade
14
Thrombosis
15
  • Definition of thrombosis
  • - Formation of a solid mass composed of the
    circulating blood elements, inside CVS system
    (blood vessels or heart) during life.

16
Causes of thrombosis
  • - There are 3 major factors which predispose to
    thrombosis (Virchows triad)
  • 1. Endothelial damage.
  • 2. Slowing turbulence of blood flow.
  • 3. Blood hypercoagulability.

17
  • 1. Endothelial damage
  • - Endothelial damage may be
  • a. Mechanical trauma, repeated tourniquet
  • b. Inflammatory arteritis, phlebitis and
    endocarditis.
  • c. Degenerative atherosclerosis, hypertension..
  • - The injured endothelium becomes swollen with
    rough surface.

18
  • 2. Slowing turbulence of blood flow.
  • - Occurs in
  • Left atrium in mitral stenosis.
  • Leg veins in varicose veins and bed-ridden heart
    failure patients.
  • Inside aneurysmal sacs.

19
  • 3. Blood hypercoagulability
  • I. Genetic (inherited)
  • Mutation of factor V gene.
  • Mutation of prothrombin gene.
  • - In both conditions the resulting factor V and
    prothrombin are not prone to degradation and have
    a sustained thrombotic actions.

20
  • Protein C and protein S deficiency
  • These are natural anti-coagulant proteins.
  • Their deficiency leads to hypercoagulability
    state.

21
  • II. Acquired
  • Prolonged bed rest or immobilization.
  • Myocardial infarction.
  • Tissue damage (surgery, fracture, burn).
  • Cancer.
  • Oral contraceptive pills.

22
Pathogenesis (Mechanism) of thrombosis
  • Endothelial injury leads to
  • 1. Exposure of sub-endothelial collagen promote
    platelet aggregation.
  • 2. Release of tissue factor promote fibrin
    formation.

23
  • I. Exposure of sub- endothelial collagen
  • a. Platelets adhesion to the exposed collagen
    (this is mediated by factor VIII released from
    endothelial cells).
  • b. Platelet activation and release of Thromboxane
    A2 (potent vasoconstrictor and induce platelet
    aggregation)

24
  • II. Release of the tissue factor (from
    endothelial cells) that stimulate the coagulation
    cascade to form thrombin that convert fibrinogen
    into fibrin.
  • The end result is fibrin network entangling
    aggregated platelet (Thrombus)

25
  • The lumen of blood vessel is occupied by a red
    mass which is adherent to the vessel wall at an
    area called the head of the thrombus .

26
Gross picture of the thrombus
27
Microscopic picture of thrombus
28
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29
  • These are "lines of Zahn" which are the
    alternating pale pink bands of platelets with
    fibrin and red bands of RBC's forming a true
    thrombus.

30
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