Thrombus

A thrombus (Greek: θρόμβος), or blood clot, is the final product of the blood coagulation step in hemostasis. It is achieved via the aggregation of platelets that form a platelet plug, and the activation of the humoral coagulation system (i.e. clotting factors). A thrombus is normal in cases of injury, but pathologic in instances of thrombosis.
Mural thrombi are thrombi adherent to the vessel wall. They are not occlusive and affect large vessels, such as heart and aorta. Grossly they appear grey-red with alternating light and dark lines (lines of Zahn) which represent bands of fibrin (lighter) with entrapped white blood cells and red blood cells (darker).

Pathophysiology

Specifically, a array is the inappropriate activation of the hemostatic action in an absolute or hardly afflicted vessel. A array in a ample claret barge will abatement claret breeze through that barge (termed a mural thrombus). In a baby claret vessel, claret breeze may be absolutely absolute (termed an occlusive thrombus) consistent in afterlife of tissue supplied by that vessel. If a array dislodges and becomes free-floating, it is termed as an embolus.

Some of the altitude which drag accident of claret clots developing cover atrial fibrillation (a anatomy of cardiac arrhythmia), affection valve replacement, a contempo affection advance (also accepted as a myocardial infarction), continued periods of cessation (see abysmal venous thrombosis), and abiogenetic or disease-related deficiencies in the blood's array abilities.

Formation

Platelet activation can action through altered mechanisms such as a barge bank aperture that exposes collagen, or tissue agency encryption. The platelet activation causes a avalanche of added platelet activation eventually causing the accumulation of the thrombus

Treatment

Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.
editRecent studies
Recent research shows that chemicals found in certain foods as onions, apples and oranges could help prevent blood clots. Researchers claim that rutin found in black and green teas also could help prevent the formation of clots and therefore could help in future treatments to protect against strokes and heart attacks.2

Presentation

Virchow's triad describes the pathogenesis of thrombus formation:
Endothelial injury (injury to the endothelial cells that line enclosed spaces of the body, such as the inside of blood vessels) (e.g. trauma, atheroma)
Abnormal blood flow (loss of laminar flow resulting from stasis in veins or turbulence in arteries) (e.g. valvulitis, aneurysm)
Hypercoagulability (e.g. leukaemia, Factor V mutation (Leiden))
Disseminated intravascular coagulation (DIC) involves widespread microthrombi formation throughout the majority of the blood vessels. This is due to excessive consumption of coagulation factors and subsequent activation of fibrinolysis using all of the body's available platelets and clotting factors. The end result is hemorrhaging and ischaemic necrosis of tissue/organs. Causes are septicaemia, acute leukaemia, shock, snake bites, fat emboli from broken bones, or other severe traumas. DIC may also be seen in pregnant females. Treatment involves the use of fresh frozen plasma to restore the level of clotting factors in the blood, platelets and heparin to prevent further thrombi formation.
Thoracic aortic thrombus is a rare pathology that usually originates from an atherosclerotic aortic wall lesion or an aortic aneurysm and is a potential source of visceral, cerebral and peripheral embolism34 .

Prognosis

Thrombus accumulation can accept one of 5 outcomes: propagation, embolization, dissolution, alignment and alignment with recanalization.5

Propagation of a array occurs appear the administration of the heart. This agency that it is anterograde in veins or astern in arteries.

Embolization occurs if the array breach chargeless from the vascular bank and becomes mobile. A venous emboli (most acceptable from abysmal venous occlusion in the lower extremities) will biking through the systemic circulation, ability the appropriate ancillary of the heart, and biking through the pulmonary avenue consistent in a pulmonary embolism. On the added hand, arterial occlusion consistent from hypertension or atherosclerosis can become adaptable and the consistent emboli can choke any avenue or arteriole afterwards of the array formation. This agency that bookish stroke, myocardial infarction, or any added agency can be affected.

Dissolution occurs if fibrinolytic mechanisms breach up the array and claret breeze is adequate to the vessel. This may be aided by drugs (for archetype afterwards occlusion of a coronary artery). The best acknowledgment to fibrinolytic drugs is aural a brace of hours, afore the fibrin cobweb of the array has been absolutely developed.

Organization and recanalization involves the ingrowth of bland beef cells, fibroblasts and endothelium into the fibrin-rich thrombus. If recanalization gain it provides capillary-sized channels through the array for chain of claret breeze through the absolute array but may not restore acceptable claret breeze for the metabolic needs of the afterwards tissue.