hematology Flashcards
when does hematopoesis begin?
early fetal development, continues throughout life–>at approx 3 week of fetal dev, clusters of specialized cells in yolk sac become blood cells
–at amount 10 weeks of gstation, hemato. shifts to liver, spleen, and bone marrow
From neonate till age five, hematopoiesis continues in the marrow of all the bones of the skeleton
After birth, the liver and spleen will stop producing blood cells
In adult, hematopoiesis continues in the pelvis, spine, ribs, cranium, and proximal ends of long bones
describe the process of heamtopoeisisisisisdiufsbdi
begins from precursor pluripotent hematopoeitic stem cells–found in bone marrow–.become uncommited hemato stem cells–> then progenitor cells–>become committed to either one cell lineage or multiple cell lineages
describe generation of RBCs
hypoxia stimulates EPO production–>essential for differentation of RBC
describe the stages of hemostasis
vascular phase–vessel sm muscle cells contract, happens neurally or chemically
–chemicals released by platelets: thromboxane A2 and serotonin (vasoconstrictors); thrombin, triggers endothelium which produces endoth. 1; also throm. A2 binds to its receptors and increases the superoxide radical conc, which binds to NO–>reduces NO vasodil effects
platelet plug formation–3 simulatenous occurences: platelet adhesion, activation, and aggregation
coagulation
describe how platelet adhesion occurs
processes mediated by binding of platelet to ligand such as von Willebrand factor; and subendothelial structures (collagen, fibronectin, laminin) (vWF is a glycoprotein found in endothel. cells, alpha-granules within platelets, and subendothel. structures)
describe platelet activation
caused by binding of platelets to ligands–is an exocytotic event; exocytose dense storage granules –> include ATP, ADP, serotonin, and Ca2+; activated platelets also release vWF, clotting factor V, and fibrinogen from alpha granules; also activated platelets initiate the breakdown of arachodonic acid to thromb. A2
Molecules released by activated platelets such as ADP , serotonin, and thromboxane A2 also amplify the platelet activation response (+ve feedback)
describe platelet aggregation
vWF released by activated platelets binds to the platelet receptor thereby activating even more platelets and allowing platelets to form molecular bridges between platelets and the subendothelial structures such as collagen
Platelet activation also induces conformational change to its membrane receptors and allowing them to have the capacity to bind fibrinogen
Fibrinogen forms bridges between platelets and participates in the process of platelet aggregation
The end result of platelet adhesion, activation, and aggregation is the formation of a platelet plug
describe the extrinsic and intrinsic coagulation pathways
The extrinsic pathway can be activated by tissue factors (tissue thromboplastin) which are released by the damaged tissue
The intrinsic pathway can be activated when coagulation factor XII comes in contact with damaged blood vessel (or negatively charged surface)
Activation of either intrinsic or extrinsic pathway then triggers a chain reaction that converts precursors into activated factors
–both pathways converge on a common pathway that ends in a fibrin clot
Extrinsic and intrinsic pathways converged into the formation of prothrombin activator
Prothrombin activator then activates prothrombin into the formation of thrombin
Thrombin then activates fibrinogen into the formation of insoluble fibrin
Thrombin also activates coagulation factor XIII which is needed to stabilize the fibrin meshwork (fibrin clot)
wehre are most coag factors synth;d?
liver
what is vit K essential for?
synth of coag factors–II, VII, IX and X
–known as anti-hemorrhagic vit
coag factor IV is Ca2+
ya
how is the clot broken down (fibrinolysis)
fibrin polymer is broken down to fibrin fragments via plasminogen–>plasmin via tPA (tissue plasminogen activator)
