Disorders of hemostasis Flashcards
5 stages of hemostasis
- vessel spasms
- formation of the platelet plug
- blood coagulation or development of an insoluble fibrin clot
- clot reaction
- clot dissolution
Disorders of hemostasis
Thrombosis- the inappropriate formation of clots within the vascular system
Bleeding- failure of blood to clot in response to appropriate stimulus
Vascular constriction
-vessel spasm constricts the vessel and reduces blood flow. It is a transient event that usually last minutes or hours
initiated by endothelial injury and caused by local humoral mechanisms
4 steps in platelet plug formation
*Adhesion and aggregation
1. attracted to a damage vessel wall
2. activation by subendothelial tissue
3. change from smooth disks to spiny spheres
4. exposing glycoprotein receptors of their surfaces
Requirements for blood clotting process
-presence of platelets produced in bone marrow
-Von Willebrand factor generated by the vessel endothelium
-clotting factors synthesized in the liver using vitamin K
Why should blood clot?
*hemostasis is designed to maintain the integrity of the vascular compartment
-Infection, volume, oxygen production, tissue damage, healing
Clot retraction and dissolution
are significant to hemostasis
-the process involves the interaction of substrates, enzymes, protein cofactors, and calcium ions that circulate in the blood or are from platelets and cells in the vessel wall
Intrinsic and extrinsic coagulation pathways
*terminal steps in both pathways are the same
Calcium, factor X and V, and platelet phospholipids combine to form prothrombin activator ->
Prothrombin activator converts prothrombin to thrombin ->
This interaction causes conversion of fibrinogen in fibrin stands that create insoluble blood clot
Regulation of blood coagulation
-Antithrombin III inactivates coagulation factors and neutralizes thrombin
-When antithrombin III is complexed with naturally occurring heparin, its action is accelerated and provides protection against uncontrolled thrombus formation on the endothelial surface
-Protein C, a plasm protein, acts as an anticoagulant by inactivating factors V and VIII
-Protein S, another plasma protein accelerates the action of protein C
-Plasmin breaks down fibrin into fibrin degradation products that act as anticoagulants
Conditions that create increased platelet function (hypercoagulability)
-atherosclerosis
-Diabetes
-smoking
-elevated blood lipoid and cholesterol levels
-increased platelet levels
Conditions that cause accelerated activity of the coagulation system
-pregnancy and the puerperium
-use of oral contraceptives
-postsurgical state
-immobility
-congested heart failure
-malignant disease
Hypercoagulability states (arterial & venous)
Arterial thrombi are associated with conditions that produce turbulent blood flow and platelet adherence
Venous thrombi are associated with conditions that cause stasis of blood flow with increased concentrations of coagulation factors
Cause of bleeding
*Decrease in the # of circulating platelets
*Impaired platelet function
Increased platelet function
-Hypercoagulability due to increased platelet function results in platelet adhesion, formation of platelet clots, and disruption of blood flow
-The causes of increased platelet function are disturbances in flow, endothelial damage, and increased sensitivity of platelets to factors that cause adhesiveness and aggregation
Thrombocytopenia
results from decreases in platelet production, increased sequestration of platelets in the spleen, or decreased platelet survival