hemostasis Flashcards
what are the 3 stages of bleeding control?
- vasoconstriction
- over in 30 min
- primary hemostasis
- platet aggregation and adhesion
- formation of temporary plug
- secondary hemostasis
- fibrin clot fomration
what stimulates vascular repair?
PDGF- platlet-derived growth factor
- this is from the activated platlets?
differentiate between the following terms
- clot
- thrombus
- emboli
- clot
- coagulation of blood at an extravascular site by vascular injury
- thrombus
- clot in the vessel lumen
- emboli
- bits of thrombus that break off and travel in the blood stream to distant sites
pick up on vasoconstriction
- how long does vasoconstriction last?
- mechanism
- lasts 30 min
- temporarily closes small vessels to stop bleeding
- platlets release
- thromboxane and serotonin(5HT
- dying endothelial cells release
- endothelin, via thrombin
- NO
- PGI2
- increase in tissue perfusion due to bloodleakage
where are platlets stored?
whats their lifespan?
stored in spleen
10 days
describe the regulation of platelet production
feedback on megakaryocytes via TPO thrombopoeitin, inducing maturation of the megakaryocytes
- platlets have a TPO membrane receptor that remove it from the blood.
- so, an increase in TPO concentration leads to and increase in platlets. a decrese leads to less platlet generation
what are the four steps to formation of platlet plug?
- what do the platlets bind to?
- what do endtothelial and megakaryoctyes secrete to assist with step 1?
- describe this cascade
- what is released by platlets? what kind of feed is this?
- platlet adhesion to collagen
- platlett membranes contain integrin receptors, when exposed to collagen they bind
- vWF asists bond
- platlets activate
- shape change, through canlicular system
- from binding to the collagen the influx of Ca, via PLc pathway
- release of : ADP, ATP, 5HT, clotting factor 5
- thrombaoxane and 5HT induce vasoconstiction and aggregattion
- shape change, through canlicular system
- platlets recruitment of other platlets
- ADP, thromboxane and 5HT start a feedforward cycle
- platlets adhering to each other
- vWF and fibrinogen receptors. fibrinogen -> fibrin
what keeps platlets away from healthy tissue?(3)
platlets not activated have a charge difference from the edothelial tissue, and the smoothness and endothelial derived protcyclin keep the platlets off
- charge
- smoothness
- enodthelial dervied prostacyclin
what is the key step in blood clotting? and what enzyme is responsible for this?
conversion of soluble plasma protein fibrinogen -> insoluble fibrin
thrombin is a key enzyme in clot formation, negtaive/positive feedback.
blood coagulation is initiated through what two pathways
both converge on the conversion of fibrinogen to fibrin
- extrinsic-common
- damage of extravascuular tissuue andendothelium
- slow
- 2-6 min
- many mechanisms to combat
- intrisic-not common
- damage of the enothelium and eposure of collagen, via toxins, pressur and chemical agents
- explosive in nature
- under 15 sec
- initiated by tissue thromboplastin
- no inhibitory mech to stop
describe the common pathway.
describe the feedback mech.
- X,V , phospholipids and Ca convert prothrombin -> thrombin
- thrombin converts
- fibrinogen ->fibrin
- factor 8 to active factor 8
- results in fibrin polymer
feedback mech
- positive feedback
- thrombin catylyzes: fibrin and F8
- activates platlets directly
how do paracrine factors influence hemostasis?
- positivly
- thrombin causes endothelial cells to release ADP, vWF
- negatively
- NO(vasodilator and antiplatlet)
- PGI2
- tissue plasminogen activator
describe the components and pathway involved in clot inhibition
- thombomodulin on endothelial cell surface, binds thrombin.
- removing thrombin from the plasma
- thrombomodulin-thrombin complex activates protein C and protein S
- activated C-S inactivate factor 5 and 8
- ttissue factor pathway inhibitor (TFPI) on cell surface inhibits protease action of factor7a
- antithrombin 3 in plasma binds to thrombin, enhanced by heparin, inactivating it
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what components are involved with fibrinolysis?
- plasminogen-> plasmin via tPA protease and urokinase
- this is the main enzyme that degrades fibrin
- digest fibers, fibrinogen, factor 5,7,8, and prothrombin