Thrombosis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Aida Javanbakht, M.D.

Overview[edit | edit source]

Irreversible formation of the blood clot is called thrombosis. This process can happen in the artery and vein ^[1].

Pathophysiology[edit | edit source]

Rudolf Virchow noted several factors affecting the clot formation, which are as follows:

1) Alterations in blood flow (stasis): Blood flows throughout the circulatory system, without significantly stopping or slowing any where. In certain pathological conditions where the blood flow slows down or stops, it causes:

• Increase in platelet to endothelium contact
• Decrease the dilution of clotting factors

This increases the risk of clot formation and form microthrombi, which further grow and propagate.

2) Injury to the vascular endothelium: Intrinsic or secondary to external trauma (eg, catheterization) can cause intimal damage and stimulates clot formation. See Coagulation.

3) Alterations in the constitution of blood (hypercoagulability): It is the propensity to develop thrombosis due to an abnormality in the system of coagulation.

These three conditions are collectively known as Virchow's triad and lead to intravascular coagulation, forming a mass of red blood cells, leukocytes, and fibrin.

Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.

Thrombus Formation[edit | edit source]

• Usually there is a balance between the coagulation and fibrinolysis systems in order to not having abnormal thrombosis in the body.
• Factors that increase the risk for a homeostatic imbalance include:

Thrombophilia

Immobilization

Trauma

• An insult to homeostatic balance can expose the sub-endothelium and lead to the collection of various coagulation factors. Accumulation of coagulation factors can lead to the formation of a thrombus of red blood cells, leukocytes, and fibrin.
• A thrombus is characteristically found to first develop in the calf veins and progressively grow in the direction of blood flow (leading to the heart).
• An exceedingly extensive thrombosis in deep veins can extend well into the iliac veins or the inferior vena cava.
• Atherosclerosis is a miss balance between lipids and the hemostasis system which caused clot in arteries. By occluding the artery myocardial infarction, stroke could happen ^[6].
• Thrombosis can happen in both Bare Metal Stent (BMS) and Drug Eluting Stent (DES).

Factors that serve as nidus for development stent thrombosis are:

Delayed endothelialization^[7][8][9].

Inflammatory response to the stent material^[10][11].

Hypersensitivity reaction around the stent material in DES serving as nidus for ST^{[12][13][14][15][16]}.

• Pregnancy increases risk of having thrombosis in both veins and arteries because of hypercoagulate state ^[17].
• Acquired risk factors for thrombosis are:

Oral contraceptive use,

Hormone replacement therapy

Advanced age

Surgery

Prolonged immobilization like hospitalization ^[18].

This video explains the process of thrombosis:

{{#ev:youtube|X_POCRsy7i4}}

Genetics[edit | edit source]

Genetic factors that play roles in causing thrombosis ^[19]:

• Non-O blood groups
• Factor V Leiden mutation
• Prothrombin G20210A gene variants
• Polymorphisms in factors IX17 or XI ^[20]

Gross Pathology[edit | edit source]

• Dull appearance.
• Zahn line from platelets and fibrin with layers of RBCs in pulmonary venous thromboembolism.
• Gross picture of thrombosis is different in live and dead person.

In live person it is gray and firm.

In dead person it is dark purple or yellow elastic called "chicken fat".

Microscopic Pathology[edit | edit source]

• lamination
• Zahn line

References[edit | edit source]

Template:WH Template:WS