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Hemostasis A protective process that provides for the rapid generation of a localized hemostatic plug at the site of a vascular injury - while maintaining clot-free blood in normal vessels.
Thrombosis
An inappropriate activation of the hemostatic process leading to the formation of a clot (thrombus) inside a blood vessels during life, obstructing the flow of blood through the circulatory system. a pathologic process
. Thromboembolism is a general term describing both thrombosis and its main complication which is embolisation.they are of variable size and shape ,depending on causes.
NORMAL HEMOSTASIS
After injury and vessel rupture
Brief period of vasoconstriction (reflex neurogenic mechanism at the arteriole level). Attraction of platelets to site of rupture attracted by the exposed subendothelial extracellular matrix.
Activation of the coagulation system (by tissue factor and secreted platelet factors); The activated coagulation system produces polymerized fibrin.
Adherent platelets + aggregated fibrin + entrapped blood cells form a hemostatic plug. Counterregulatory mechanisms are activated to limit propagation of the hemostatic plug to the injury site.
HEMOSTATIC SYSTEM
INTRINSIC
PATHWAY
COMMON PATHWAY EXTRINSIC PATHWAY
PLATELETS
CLOT
COLLAGEN
TISSUE FACTOR
VESSEL WALL
Causes
Classically, thrombosis is caused by abnormalities in one or more of the following (Virchow's triad): Changes in the composition of the blood favouring platelet aggregation and fibrin formation (hypercoagulablility). Quality of the vessel wall(endothelial damage or altered endothelial function) eg.thrombi on endocardium , MI ,or
ulcerated atheromatous plaques in artery walls.bacterial toxin.
stasis as in polycythemia or aneurysms results in loss of laminar blood flow and allow platelets to adher to the endothelium also allow the local accumulation of activated coagulation factor.turbulence causes reduction in endothelial PGI2 and tPA formation
Virchows TRIANGLE
ENDOTHELIAL INJURY
THROMBOSIS
HYPERCOAGULATION
ENDOTHELIAL INJURY
any perturbation in the dynamic balance of the pro- and antithrombotic effects of endothelium, not only physical damage
ANTI-Coagulant PROPERTIES
Membrane HEPARIN-like molecules Makes THROMBOMODULIN Protein-C TISSUE FACTOR PATHWAY INHIBITOR
PROTHROMBOTIC PROPERTIES
Makes vWF, which binds PlatsColl Makes TISSUE FACTOR (with plats) Makes Plasminogen inhibitors
1 HYPERCOAGULABILITY
(INHERITED)
2 HYPERCOAGULABILITY (ACQUIRED)
Prolonged bed rest or immobilization Myocardial infarction Atrial fibrillation Tissue damage (surgery, fracture, burns) Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis) Prosthetic cardiac valves Disseminated intravascular coagulation Heparin-induced thrombocytopenia Antiphospholipid antibody syndrome (lupus anticoagulant syndrome) Cardiomyopathy Nephrotic syndrome Hyperestrogenic states (pregnancy) Oral contraceptive use Sickle cell anemia Smoking, Obesity
ACUTE MYOCARDIAL INFARCTION = OLD ATHEROSCLEROSIS + FRESH THROMBOSIS ARTERIAL THROMBI also may send fragments DOWNSTREAM, but these fragments may contain flecks of PLAQUE also LODGING is PROPORTIONAL to the % of cardiac output the organ receives, i.e., brain, kidneys, spleen, legs, or the diameter of the downstream vessel
ARTERIAL/CARDIAC THROMBI
Atherosclerosis
is characterized by intimal lesions called atheromas, or atheromatous or fibrofatty plaques, that protrude into and obstruct vascular lumina, weaken the underlying media, and may undergo serious complications.
ATHEROSCLEROTIC PLAQUE
NORMAL ARTERY
ATHEROSCLEROTIC PLAQUE
15
remaining lumen
calcified area
Thrombus Causing MI
Sequels of Block
Collateral circulation: Ischemia, Infarction, Gangrene Haemorrhage
Fate of thrombus
Spread (propagation) Accumulation of more
platelets and fibrin, becoming larger
thrombi may induce inflamation and fibrosis(organization)and may eventually recanalized or they may be incorporated into a thickened vascular wall.