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Blood plasma proteins, coagulation, and fibrinoylsis
GMC - 8/22
Terms in this set (35)
property of plasma. process by which fibrinogen is converted into insoluble fibrin.
series of physiologic processes that prevent bleeding when a blood vessel is damage, while simultaneously keeping blood in a fluid state. requires a continuous and dynamic interaction of blood vessels, platelets, and plasma coagulation factors.
balance between bleeding and clotting
formation of a blood clot, as part of hemostasis. also form to repair damage to the endothelial lining.
what are the major functions of endothelial cells?
1. inhibition of platelet aggregation
2. inhibition of coagulation
3. activation of fibrinolysis
non-nucleated cells in the blood; major role is to form mechanical plugs at the site of vessel injury; secrete regulators of the clotting process and vascular repair. produce coagulation factors
other functions of platelets
control the vessel wall growth, secrete growth factors, important in vascular tone, involved in control of blood flow and blood pressure, leukocyte traffic
what do endothelial cells secrete?
PGI2 (procyclin) (prostaglandin I2)
NO (nitric acid)
not involved in forming a clot; plasma membrane invaginates extensively into the interior of the cell, forming an open membrane system. this structure increases membrane surface area available for clotting reactions. interior contains microfilaments and extensive actin/myosin system
activation of platelets
response to endothelial injury; causes Ca dependent changes in contractile elements; change the plasma membrane. long pseudopodia are generated, increasing the surface area as clot formation is initiated. secrete thromboxane A2
3 types of granules in platelets
contain serotonin, ADP, and calcium.
*delta symbol looks like a SAC.
contains heparin, platelet-derived growth factor, beta-thromboglobulin, fibrinogen, von Willebrand factor, and other clotting factors
contain hydrolytic enzymes; modulate platelet aggregation and clotting
modulates/inhibits thrombin. secreted by endothelial cells
inhibited by thrombomodulin. activated form of factor II (prothrombin). catalyzes the conversion of fibrinogen to fibrin
inhibits 2 different coagulation factors (FVa and FVIIIa). regulatory protein. regulated by proteolytic cleavage, and when activated, it is itself a serine protease.
secreted by endothelial cells; together with antithrombin, inhibits thrombin and FXa
protein that circulates in the blood and is found in platelet granules. activated by thrombin to convert to fibrin.
consists of 2 triple helices held together with disulfide bonds. necessary for aggregation
activation of fibrinoylsis
tPA (and urokinase) activates plasminogen into plasmin.
plasmin degrades fibrin into fibrin degradation productions (end of coagulation)
hemostatic plug formation
primary and secondary process.
primary: aggregation-->platelet aggregation-->clotting
clotting and fibrin together make the hemostatic clot.
missing endothelial cells, so there is no secretion of PGI2 and NO. so no vasodilation. vasoconstriction occurs. endothelins are present, and they produce more vasoconstriction.
damage also secretes vWF
von Willebrand factor. synthesized in endothelial cells. platelets bind to this at the injury site. when that happens, glycoprotein (GPIba) on the platelet surface is activated.
bleeding disorder caused by defects in GPIb. platelet aggregation is affected, because of the inability of GPIb to adhere to vWF
which coagulation factors require vitamin k for activation? why?
factors 2, 7, 9, 10. these have a glutamic acid residue that produces gamma-carboxyglutamate residues. theres are proenzymes. calcium can interact with these to bring the proenzymes to the membrane and coagulate.
works as a platelet aggregator and vasoconstrictor
extrinsic, intrinsic, and common.
soluble fibrinogen is converted to insoluble fibrin to reinforce the plug
stimulated by an external stimuli (such as blunt trauma). damaged tissues present tissue factor to the blood at the injured site. FVII binds to tissue factor, autocatalyzes to FVIIa which then activates FX to FXa. requires access to membranes and calcium. FVa and VIIIa serve as sites for assembling enzyme-cofactor complexes on the platelet surface-->thrombin formation--> fibrinogen-->fibrin. cross linking occurs with FXIIIa = cross-linked (hard) clot.
does the same as extrinsic only longer.
FXIIa --> XIa --> IXa which then activates FX to FXa. requires access to membranes and calcium. FVa and VIIIa serve as sites for assembling enzyme-cofactor complexes on the platelet surface-->thrombin formation--> fibrinogen-->fibrin. cross linking occurs with FXIIIa = cross-linked (hard) clot.
once they both get to factor X, it activates prothrombin (which needs calcium and phospholipids and factor V). gets fibrin and that with factor XVIIIa makes the cross-linked hard clot.
what is the final product of plasminogen pathway?
plasminogen --tPA--> plasmin --> fibrin --> fibrin degradation products
vitamin K deficiency
thrombocytopenia (platelet deficiency)
vitamin k deficiency
vitamin k is necessary for liver formation of 5 important factors: prothrombin (FII), FVII, FIX, FX, and protein C. without vitamin k, insufficiency of these coagulation factors in the blood can lead to serious bleeding tendencies.
in 85% of cases, caused by an abnormality of deficiency of FVIII; hemophilia A (classic hemophilia). other 15%, bleeding tendency is caused by deficiency of FIX. almost exclusively in males
presence of very low numbers of platelets in the circulating blood. bleed from small venules or capillaries, rather than from larger vessels (as in hemophilia). no platelets are around to form the initial clot.
what maintain the integrity of the circulatory systems?
plasma proteins in association with platelets
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