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Biology 2313 Week 3 Notes

by: Ednjon Parilla

Biology 2313 Week 3 Notes Biology 2313

Ednjon Parilla
GPA 3.9

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Notes from the lecture given on Sept. 7th
Human Anatomy & Physiology II
Dr. Zaineb Al-Dahwi
Class Notes
Biology, anatomy, Physiology, Human, Anatomy & Physiology II, Blood, Hemostasis, Coagulation, Platelets, Science, health
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This 4 page Class Notes was uploaded by Ednjon Parilla on Saturday September 10, 2016. The Class Notes belongs to Biology 2313 at University of Texas at El Paso taught by Dr. Zaineb Al-Dahwi in Fall 2016. Since its upload, it has received 72 views. For similar materials see Human Anatomy & Physiology II in Science at University of Texas at El Paso.


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Date Created: 09/10/16
Blood: Hemostasis & Coagulation  Platelets  Contain chemicals which are needed for blood clotting 2+  ADP, Ca , Serotonin, Actin, Myosin  Not adherent; endothelium  Releases chemicals which PREVENTS adherent inner lining of tissue o Other chemicals PROMOTE adherence  Lifespan: 10-15 days (short)  Long lifespan if they help in the formation of a blood clot  Production Pathways of Platelets  Activated by the glycoprotein hormone Thrombopoietin  Produced by liver and kidney (mostly liver)  This activation activates different production pathways  Procedure 1) Megakaryoblast  Stage I: Megacryocytes o Committed cells express surface receptors 2) Promegakaryote  Stage II/III: Megalokaryocyte o Undergo mitotic divisions o Nucleus grows huge 3) Megalokaryocyte  Stage IV: Platelet o Nucleus gets larger o No division of cytoplasm of cell  Cytoplasm divides into compartments; called Compartmentalization  Cytoplasmic extensions adhere to capillaries (have openings to connect to the extensions)  Extensions are pushed into capillaries  Extensions are broken down and turn into platelets  Homeostasis = Formation of Platelets/Stating the Bleeding PHASE ONE  3 Events 1) Vascular Spasm/ Vasoconstriction o Decrease of diameter  Decreases the blood flow  Increases resistance o Damage of collagen factors 2) Platelet Plug Formation o Release Reaction i. Nucleus enlarges ii. Shape changes from disc to having cytoplasmic extensions to adhere to each other iii. Become sticky iv. Release ADP; aggregating agent which attracts platelets that are running in the blood v. Serotonin and Thromboxane also serve as attractants for restricting and more aggregation of platelets ↳Disease that occurs during the Platelet Plug formation: Von Willebrand Factor which PREVENTS the formation of a “bridge” between platelet and collagen fiber 3) Coagulation: Formation of Blood Clot o Coagulation reinforces the platelet plug by adding fiber strands  Begins with the activation of plasma proteins, which are circulating as inactive  Once tissue is damaged they become activated by triggering other factors such as: o Changing plasma proteins to enzyme chemicals by clipping a piece of the protein  Roman numeral numbering is based on the order of discovery, not sequence of events o 2 places where blood clotting can occur  Outside; Intrinsic pathway  Inside; Extrinsic pathway  Similarities a. Both lead to formation of factor 10; formation of Prothrombin Activator b. Sequence of chemical events; activation depends on exposure to negatively charge membranes/surfaces (activated platelets)  Differences a. Intrinsic:  Blood clotting factor are within the blood  Triggered by exposure to negative charged surfaces, activated platelets, collage fibers, and glass  Pathway is initiated and activated inside blood b. Extrinsic  Factor promoting mechanism is outside the blood  Triggering factor is the Tissue Factor - Tissue surrounding the blood vessel (outside epithelium of blood vessel wall)  Shorter than the Intrinsic pathway ↳Example: Blood in a beaker Provided negative surface would be the beaker itself, the blood clotting factor is in the blood, and the tissue factor is NOT available Intrinsic Pathway PHASE TWO  Prothrombin Activator: changes into the thrombin enzyme (plasma protein) PHASE THREE  Converting Soluble into Insoluble (liquid to gel-like solid)  Fibrinogen (soluble) uses the enzyme thrombin to be converted from a plasma protein to Fibrin molecules which form cross-linked Fibrin Strands o Fibrin strands are bundled together to create the Fibrin Mesh Fibrin mesh is a network of fibrin strands that trap blood cells  Clot Retraction  Platelet induced process  Clot becomes smaller; it’s easier to get rid of o PDGF  Fibroblast  CT o VEGF  Endothelial Cell Endothelium (skin)  Platelets contain Ca , actin, and myosin = capable of contraction o Use of calcium allows contraction without action potential o Serum is being squeezed out of clot while contracting Serum is the plasma minus the clotting factors, which stay in the blood  2 Pathways: 1) Platelet Derived Growth Factor (PDGF; release of chemicals) Promotes the repair process  Fibroblasts (fiber forming cells) are activated in order to rebuild collagen fibers and connective tissue in the wall 2) Vascular Endothelial Growth Factor (VEGF)  Released chemicals from epithelial cell (LPA is the same as epithelial cell)  Activates cells to go through mitosis  Fibrinolysis: Digestion of Clot (digestion of fibrin mesh)  Plasminogen is the plasma protein incorporated in the clot  Activation starts with the digestion  Tissue Plasminogen Activator activates plasminogen which is then converted into plasmin (enzyme)  Red Blood Cells  ABO Blood Groups  Humans are classified by glycoproteins which is on the surface of RBC  Antigen: foreign to the blood


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