Why Unwanted clot formation occur in healthy vessels?

Why Unwanted Clot Formation Occurs In Healthy Vessels?

Introduction

     As we know that clot formation occurs only when there is an injury to the vessels, but it also occurs in some cases in the healthy vessels where it's termed as Thrombus.

Also read :How Vitamin-K helps in Coagulation (Clotting) ?

What is Thrombosis?

     A blood clot is formed within the vascular system due to the activation of Procoagulation factors. If that formed clot blocks the vein or artery, then that's called Thrombosis, and that clot is called Thrombi. Mostly it occurs in veins.

Normally Which Factors Prevent Thrombosis?

      There are a number of factors that inhibit or prevent thrombosis, and are categorized into three groups named as:

• Anti-Platelet Factors:  This includes Nitric Oxide, Prostacyclin, and Adenosine diphosphate.
• Anti-Coagulation Factors:  This includes heparin that acts as a cofactor for AT-III that inhibits the factor-II, IX and X. Also there is another named Thrombomodulin released by endothelial cells that bind Thrombin with itself, then Thrombin activates Protein-C that functions as an inhibitor of Factor-V and VIII.
• Anti-Fibrinolytic Factors:  It includes the Tissue Plasminogen Factor (tPA) that is released by endothelial cells, it functions to degrade the Plasmin, Fibrinogen, and other blood cells present in the clot.

 

Why Clot Formation occurs in Healthy Vessels?

     The triad that includes the causes, why a clot is formed in healthy vessels is called Virchow's Triad. It includes three causes of Thrombosis, which are given below:

• Endothelial Injury
• Alteration in normal blood flow
• Hypercoagulability 

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Endothelial Injury

     As endothelial integrity is the main factor to maintain blood flow, so defect to that Integrity is called Endothelial Injury, and ultimately it leads to Thrombus Formation.

     The causes of Endothelial Injury includes Cigratte smoke, Hypoxia, Inflammatory conditions, Ulcetrated atherosclerotic plaques, Radiations and Homocysteinemia (elevated homocysteine in the blood).

     As the endothelial injury occurs, it leads to the adhesion of platelets to that area, then the fibrin deposition occurs, then all the blood cells including RBC and WBCs are entrapped there and ultimately turbulence occurs. The dysfunctional endothelial cells release more procoagulants that causes more coagulation.

Also read :Cardiac Tamponade-What it is and How to Diagnose It

Alteration in normal blood flow

     Normally, the blood has a laminar flow, means blood plasma flows peripherally while all formed elements flow centrally so that platelets can not come in contact with endothelial wall. 

     Alteration in blood flow may occur due to two reasons:

• Turbulence: When turbulence occurs, it causes a counter-current and causes endothelial injury, and ends the separation between platelets and endothelial wall, so activates the coagulation. If Atherosclerotic plaques are formed, then they lead to the narrowing of that lumen so causes turbulence. If Ulcerated Atherosclerotic plaques formed, then both turbulence and endothelial injury occur.
• Stasis: Stasis is the stagnant blood flow. It is the major contributor to Venous thrombi development. It induces thrombi by enhancing the activity of procoagulants, so ultimately anticoagulants effects are diluted.

Hypercoagulability

     Hypercoagulability is an any alteration in the coagulation cascade that predisposes to thrombosis. It is the less frequent thrombosis contributor. The causes of Hypercoagulability are categorized into Primary and Secondary causes.

     1) Primary Causes (Genetic): The primary causes are those that can be transmitted hereditarily, and it includes: 

• Factor-5 leiden mutation
• Prothrombin mutation
• Sticky Platelet Syndrome
• Elevated factor-VIII IX, XI and Fibrinogen

     2) Secondary Causes (Acquired): The secondary causes are those that can be acquired during the life. These are:

• Disseminated Intravascular Coagulation
• Prolonged Bed Rest
• Tissue Injury
• Myocardial Infarction
• Cancer
• Heparin-Induced Thrombocytopenia
• Anti-phospholipid antibody Syndrome

     The hepatic disease can lead to the increase in production of Prothrombin, if their is less production of Bile, then it leads to the decrease in absorption of Vitamin-K.

Also read :Blood Transfusion: Steps, Types, Complications and its Necessity

Types of Thrombus

      The characteristics of the thrombus include the lines of Zahn that are alternating layers of platelet-fibrin giving pallor appearance and Red cells giving a Darker appearance. Thrombi may be Arterial, Venous, and Mural, as the difference is only due to the site of thrombi. 

• Venous Thrombi: If thrombus is formed in venous, that mostly occurs, then called Venous Thrombi. The sites of venous thrombi are Superficial Varicose Veins, Deep leg veins.
• Arterial Thrombi: When a thrombus is formed in the artery, then it's termed Arterial Thrombi. The sites of arterial thrombi include Femoral artery, Coronary artery, and Cerebral artery.
• Mural Thrombi: When a thrombus is formed whether in heart chambers or in the aortic lumen, that Thrombi is called Mural Thrombi. The Arrythmia, Dilated Cardiomyopathy (DCM), and Myocardial Infarction (MI) are the causes of Cardiac Mural Thrombi, while the causes of Aortic Mural Thrombi includes Ulcerated Atherosclerotic plaques and Aneurysm.

 What are Vegetations?

     The formation of Thrombi in the valves of the heart is termed as Vegetations. When the bloodborne bacteria/fungi adhere with the previously affected valves or healthy valves, it causes endothelial injury and turbulence that leads to the formation of Thrombus in valves. 

     Sterile Vegetations can occur in non-infected valves due to the hypercoagulable state of a person, that is called Non-bacterial thrombotic Endocarditis.

Fate of Thrombi

     Following are the fates of Thrombi, that are given below:

• Propagation:  Thrombi accumulate more platelets and fibrin, that leads to the increase in its size.
• Embolization: As the thrombi formation is completed, then its dislodging occurs and then it travels to other sites.
• Dissolution: If the thrombi is smaller, then fibrinolysis can occur and its destroyed. But if older thrombi become resistant to fibrinolysis due to extensive fibrin deposition. then this problem is resolved by using fibrinolytic drugs.
• Organization and Recanalization: The older thrombi become organized by the ingrowth of endothelial cells, and smooth muscles.

Conclusion 

     If clot formation occurs due to a vascular injury, then its good. But if it occurs in a healthy vessels, then it's dangerous.