Haemostasis and Thrombosis - labsstudies

Haemostasis and Thrombosis

Haemostasis and Thrombosis

 Meaning of Haemostasis and Thrombosis 

Haemostasis

  • Is the process of preventing excessive blood loss in the body.
  • Normal hemostasis is the result of tightly regulated processes that keep blood in normal vessels fluid and clot-free while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
  • There are three primary mechanisms used to control bleeding: vascular spasm, platelet plug, and blood clotting.

Thrombosis

  • Is the formation of a blood clot that either completely or partially blocks a blood vessel.
  •  The thrombus can cause infarction, or tissue death, due to a blocked blood supply.
  • Thrombosis is the pathologic form of haemostasis. It involves the formation of a blood clot (thrombus) in uninjured vessels or the thrombotic occlusion of a vessel after a relatively minor injury.
  • The vascular wall, platelets, and the coagulation cascade are all involved in hemostasis and thrombosis.

 Risk Factors of Thrombosis

The following are risk factors of thrombosis:

  •  Obesity
  •  Varicose Veins
  •  Immobility
  •  Pregnancy
  •  High estrogen levels
  • Previous history of DVT
  • Surgery and trauma of the pelvis and lower limbs
  • Age
  •  Heart failure
  •  Recent myocardial infarction
  • Lower limb paralysis
  •  Cigarette smoking

 

Thrombosis Pathogenesis and Causes

Both haemostasis and thrombosis involve three components, which are:

  1.  Vascular spasm
  2.  Platelet plug 
  3.  Coagulation cascade 

1. Vascular spasm

  • It occurs when a blood vessel is punctured.
  • The smooth muscle surrounding the vessel contracts, cutting off blood supply to the area.

2. Platelet Plug Formation

  • It is a more complex process than vascular spasm and occurs in three stages:

o Platelet adhesion

  • When platelets detect damage to a blood vessel, they begin to adhere to the exposed surfaces.

o Platelet release reaction

  • Once attached to a site of damage, platelets begin to change.
  • They create extensions so that they can communicate with one another, and then they publish their contents, which contain clotting factors, growth factors, fibroblasts, ADP, ATP, calcium ions, and serotonin.

o Platelet aggregation

  • The ADP causes nearby platelets to become sticky and adhere to the other recruited platelets.
  • When the collection is large enough, it forms a platelet plug, which prevents blood loss through holes in small vessels.

 3. Coagulation cascade 

  • Clotting, also known as coagulation, is the most complex haemostatic process.
  • Its goal is to convert liquid blood into a gel, which is composed of protein fibers called fibrin in which the formed elements of blood are trapped.
  • The gel effectively forms a cap over a wound.
  • When blood clot is involve several substances known as clotting factor.
  • The clot that forms over a broken area prevents blood loss, and the fibrin within the clot contracts, assisting in pulling the broken ends of the blood vessel back together.
  • Tissue repair can occur once the ends are retracted; however, homeostatic imbalances and clot formation can occur despite these mechanisms.
  • Atherosclerotic plaque, trauma, or infection can roughen the insides of blood vessels, attracting platelet adhesion.
  • Clotting in an unbroken vessel is referred to as thrombosis, and the clot itself is referred to as a thrombus.

Thrombosis Pathogenesis

The Virchow’s Triad is involved in the pathogenesis of thrombosis, which includes:

 Endothelial injury

  • Examples include trauma, surgery, endotoxins, and cigarette smoke.

Improper blood flow

  • Prolonged immobilization, cardiac failure, aneurysms, and cardiac arrhythmias are all possibilities.

 Hypercoagulability condition

  • Changes in blood hormones or biochemistry, pregnancy, oral contraceptives, cancer, polycythaemia, sickle cell disease.

Arterial thrombi grow retrogradely from the point of attachment, whereas venous thrombi grow in the direction of blood flow (thus both tend to propagate toward the heart).

 Also read: Jaundice

Thrombi Morphology and it is Types

  • Thrombi can form anywhere in the cardiovascular system, including cardiac chambers, valves, arteries, veins, and capillaries.

Thrombi Morphology

  • The size and shape of a thrombus are determined by its location and cause.
  • Arterial or cardiac thrombi usually start at sites of endothelial damage or turbulence.
  • Venous thrombi are most commonly found at sites of stasis (sluggish blood flow).
  • Lines of Zahn are grossly (and microscopically) visible laminations in thrombi that represent pale platelet and fibrin layers alternating with darker erythrocyte rich layers. These lines are significant because they represent thrombosis in the context of flowing blood; their presence can thus potentially distinguish ante-mortem thrombosis from the bland non-laminated clots that occur in the post-mortem state.

Types of Thrombi

a. Mural thrombi

  • Thrombi in the heart chambers or the aortic lumen.

 b. Arterial thrombi

  •  These occur in the arteries and are frequently occlusive and are produced by platelet and coagulation activation.
  • They are typically a friable meshwork of platelets, fibrin, erythrocytes, and degenerating leukocytes.

c. Venous thrombosis (phlebothrombosis)

  • Occur along veins and are almost invariably occlusive, and the thrombus can create a long cast of the lumen.
  • Platelets play a secondary role as a result of activation of the coagulation cascade.
  • Because these thrombi form in the slow venous circulation, they tend to contain more enmeshed erythrocytes and are thus referred to as red, or stasis, thrombi.
  • Deep venous thrombosis (DVT) is an example of a vein embolism.

d.  Post-mortem clots

  • Post-mortem thrombi are gelatinous, with a dark red dependent portion where red cells have settled by gravity and a yellow ‘chicken fat’ supernatant, and they are usually not attached to the underlying wall.
  •  In contrast, red thrombi are firmer and more focally attached, with strands of gray fibrin visible when sectioned.
  •  Bacterial or fungal blood infections can damage valves, leading to large thrombotic masses (infective endocarditis).
  • Sterile vegetations can also form on non-infected valves in hypercoagulable states, a condition known as nonbacterial thrombotic endocarditis.

Thrombi’s fate

If a patient survives the initial thrombosis, thrombi will undergo some combination of the four events listed below in the days or weeks that follow:

  •  Dissolution
  • Propagation
  •  Embolization
  • Organization and recanalization

Dissolution

  • Fibrinolytic activity may be used to treat thrombosis.
  •  Dissolution is caused by fibrinolytic activation, which results in rapid shrinkage and, in extreme cases, total lysis of recent thrombi.
  •  In older thrombi, extensive fibrin polymerization makes the thrombus significantly more resistant to proteolysis, making lysis ineffective.
  •  This is clinically significant because fibrinolytic agents are used to treat patients.

Propagation

  • Thrombus may accumulate more platelets and fibrin, eventually leading to vessel obstruction.

Embolization

  •  It may dislodge and travel to other parts of the vessel.

Thrombus organization and recanalization

  • Thrombus may induce inflammation and fibrosis and eventually re-canalized.

 

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