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Hematopoeisis and Hemostasis
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Hematopoiesis The process of blood cell formation
Includes all blood cells- red and white Occurs in red bone marrow from stem cells known as hemocytoblasts Hemocytoblast differentiation Lymphoid stem cell produces lymphocytes Myeloid stem cell produces all other formed elements © 2015 Pearson Education, Inc.
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Figure 10.4 The development of blood cells.
Hemocytoblast stem cells Lymphoid stem cells Myeloid stem cells Secondary stem cells Basophils Erythrocytes Platelets Eosinophils Lymphocytes Monocytes Neutrophils
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Production controls over formed elements
Because RBCs are anucleate they cannot divide, grow, or synthesize proteins Life span of 100 to 120 days phagocytes in the spleen/liver eliminate remains New RBCs produced by hemocytoblasts in the red bone marrow (a 3-5 day process) © 2015 Pearson Education, Inc.
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Control of Erythrocyte Production
erythropoietin : hormone that controls RBC production rate Produced by kidneys in response to O2 levels Targets bone marrow to mfr RBCs negative feedback maintains blood oxygen levels (see figure 10.5 on page 346) works by increasing/decreasing erythropoietin release © 2015 Pearson Education, Inc.
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Figure 10.5 Mechanism for regulating the rate of RBC production.
Slide 1 IMBALANCE Homeostasis: Normal blood oxygen levels 1 Stimulus 5 O2–carrying ability of blood increases. Low blood O2–carrying ability due to • Decreased RBC count • Decreased amount of hemoglobin • Decreased availability of O2 IMBALANCE 4 Enhanced erythropoiesis increases RBC count. 2 Kidney (and liver, to a smaller extent) releases erythropoietin. 3 Erythropoietin stimulates red bone marrow.
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Production of WBCs and Platelets
A group of Colony stimulating factors (CSFs) and interleukins prompt bone marrow to generate leukocytes CSFs are specific to the types of WBCs they act on used to stimulate cell production in cancer patients undergoing chemo or radiation therapy Hormone thrombopoietin stimulates production of platelets from megakaryocytes © 2015 Pearson Education, Inc.
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Hemostasis- blood clotting
involves three phases: Vascular spasms Platelet plug formation Coagulation (blood clotting) © 2015 Pearson Education, Inc.
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Vascular Spasms Vasoconstriction causes blood vessel to spasm
Narrowing of the blood vessel Slows blood loss © 2015 Pearson Education, Inc.
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Figure 10.6 Events of hemostasis.
Slide 2 Step 1 Vascular spasms occur. Smooth muscle contracts, causing vasoconstriction.
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Platelet Plug Formation
Collagen fibers are exposed by a break in a blood vessel Platelets become “sticky” and cling to fibers Anchored platelets release chemicals to attract more platelets A positive feedback mechanism Platelets pile up to form a platelet plug (white thrombus) © 2015 Pearson Education, Inc.
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Figure 10.6 Events of hemostasis.
Slide 3 Step 2 Platelet plug forms. Injury to lining of vessel exposes collagen fibers; platelets adhere. Collagen fibers Platelets release chemicals that make nearby platelets sticky; platelet plug forms. Platelets
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Coagulation Clotting factors in blood plasma and injured tissue cells interact with Ca²⁺ to produce the enzyme thrombin Thrombin catalyzes the joining of fibrin molecules to make a meshwork that traps RBCs and platelets This forms the clot, which is broken down after repair of damaged tissue This mechanism is controlled so that the presence of the clot inactivates the factors that initiated the response To avoid clotting of all blood in the body cascade.html © 2015 Pearson Education, Inc.
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Figure 10.6 Events of hemostasis.
Slide 4 Step 3 Coagulation events occur. Clotting factors present in plasma and released by injured tissue cells interact with Ca2+ to form thrombin, the enzyme that catalyzes joining of fibrinogen molecules in plasma to fibrin. Fibrin Fibrin forms a mesh that traps red blood cells and platelets, forming the clot.
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Figure 10.7 Fibrin clot.
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Undesirable Clotting Thrombus Embolus Potential causes:
A clot in an unbroken blood vessel Can be deadly in areas such as the heart Embolus A thrombus that breaks away and floats freely within the bloodstream Potential to clog vessels in critical areas Potential causes: Burns Physical blows Fatty material (plaque) Slow blood flow © 2015 Pearson Education, Inc.
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Bleeding Disorders Thrombocytopenia Liver problems Hemophilia
Platelet deficiency Results from bone marrow suppression Cancer, radiation, drugs, autoimmune condition, bacteria Evidenced by petechiae (purplish skin blotches) Liver problems due to cirrhosis, hepatitis, or low Vitamin K stores Liver synthesizes the clotting proteins Hemophilia Hereditary bleeding disorder Normal clotting factors are missing © 2015 Pearson Education, Inc.
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