Hemostasis and Coagulopathies
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Last updated 3:30 AM on 9/14/23
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35 Terms
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Composition of blood
\-Plasma
\-Blood Cells
\-Thrombocytes(platelets)
\-Leukocytes
\-Blood Cells
\-Thrombocytes(platelets)
\-Leukocytes
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plasma proteins
immune systems
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Erythrocytes
RBCs
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\#of oxygen hemoglobin carry
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platelets
help with clotting
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leukocytes
white blood cells
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pluripotent stem cells
\-makes multiple cell types
\-master cells
\-make blood cells from 3 types of body tissue
\*can self renew
\-master cells
\-make blood cells from 3 types of body tissue
\*can self renew
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myeloid stem cells
circulate in blood
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Hemostasis
ability to clot blood
*specifically the lining of a blood vessel
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platelet storage
spleen
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megakaryocytes
large fragment in bone marrow responsible for creating platelets
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thrombopoetin
platelet production
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place of platelet formation
liver, kidney, smooth muscle, bone marrow
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Plasma protiens
\-circulate as inactive procoagulation factors
\-most synthesized by liver
\-von Willebrand factor made by megakaryocytic and endothelium
\-most synthesized by liver
\-von Willebrand factor made by megakaryocytic and endothelium
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calcium factor
works with other clotting factors as a co clotting factor
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vWF
platelet adhesion
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ADP, TXA2
platelet aggregation
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calcium
coagulation cascade
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COX-1
catalyzes production of thromboxane A2
\-present in most tissues in the body especially GI tract protects from digestive juices
\-present in most tissues in the body especially GI tract protects from digestive juices
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COX-2
catalyzes production of prostacyclin
\-sites of inflammation
\-sites of inflammation
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anticoagulant
\-prevents clots
\*not break down clots
\*not break down clots
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vessel spasm
restricts blood flow to prevent blood loss
allows epithelial later to start healing
allows epithelial later to start healing
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formation of platelet plug
\*platelets arrive quickly
\-von Willebrand factor is released by epithelial lining
\-bind to receptors on collagen fibers to form plug
\-von Willebrand factor is released by epithelial lining
\-bind to receptors on collagen fibers to form plug
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blood coagulation
prothrombin→ thrombin turns fibrinogen→ fibrin
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interinsic factor
\-begins in circulation
\*initiated by C12
\*initiated by C12
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extrinsic pathway
\-release mediators when agitated
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clot retratction
-repair epithelial lining
-fibrin threads will be stretched and will squeeze plasma out of wounds
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plasminogen
forms within clot while clot forms
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Clot lysis
Plasminogen activators will turn plasminogen→ plasmin which will digest fibrin
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hypercoagulation
\-extreme blood clot
\-overcoagulation
\-overcoagulation
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thrombocytopenia
decrease production
increased destruction
platelets used up in formed clots
increased destruction
platelets used up in formed clots
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coagulation disorder
impaired platelets functions
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von willebrand diesease
decrease platelets adhesion
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disseminated intravascular coagulation
unregulated thrombin explosion
\-too much tissue factor
\-leads micro vascular thrombosis and target organ damage
\-too much tissue factor
\-leads micro vascular thrombosis and target organ damage
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platelets disorder
bleeding diesease