Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hematopoiesis  Blood cell formation  Occurs in red bone marrow  About one ounce a day (100 billion cells)  All blood cells are derived from a common stem cell (hemocytoblast)  Hemocytoblast differentiation  Lymphoid stem cell produces lymphocytes  Myeloid stem cell produces all other formed elements

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4 Hematopoiesis

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4, step 1 Formed Elements Hemocytoblast stem cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4, step 2 Formed Elements Hemocytoblast stem cells Secondary stem cell Lymphoid stem cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4, step 3 Formed Elements Hemocytoblast stem cells Secondary stem cell Lymphocytes Lymphoid stem cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4, step 4 Formed Elements Hemocytoblast stem cells Secondary stem cells Lymphocytes Lymphoid stem cells Myeloid stem cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4, step 5 Formed Elements Hemocytoblast stem cells Secondary stem cells Basophils Eosinophils NeutrophilsMonocytesLymphocytes Erythrocytes Platelets Lymphoid stem cells Myeloid stem cells

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formation of Erythrocytes  Once accumulated enough hemoglobin, they eliminate organelles and nucleus and therefore become unable to divide, grow, or synthesize additional proteins  Young RBC – reticulocyte for two days  Wear out in 100 to 120 days  When worn out, RBCs are eliminated by phagocytes (Monocytes) in the spleen or liver  Lost cells are replaced by division of hemocytoblasts in the red bone marrow

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production  Rate is controlled by a hormone (erythropoietin)  Kidneys produce most erythropoietin as a response to reduced oxygen levels in the blood  Homeostasis is maintained by negative feedback from blood oxygen levels

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Increased O 2 - carrying ability of blood Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 1 Normal blood oxygen levels

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 2 Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 3 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 4 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Kidney releases erythropoietin Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 5 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Erythropoietin stimulates Kidney releases erythropoietin Red bone marrow Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 6 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 7 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Increased O 2 - carrying ability of blood Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 8 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Increased O 2 - carrying ability of blood Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels Imbalance

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formation of White Blood Cells and Platelets  Controlled by hormones  Colony stimulating factors (CSFs) and interleukins prompt bone marrow to generate leukocytes  Thrombopoietin stimulates production of platelets

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  “Stoppage of bleeding” resulting from a break in a blood vessel  Hemostasis involves three phases  Vascular spasms  Platelet plug formation  Coagulation (blood clotting)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Fibrin Clot

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.6 Hemostasis

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Vascular spasms  Vasoconstriction causes blood vessel to spasm  Spasms narrow the blood vessel, decreasing blood loss

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6 Injury to lining of vessel exposes collagen fibers; platelets adhere Fibrin clot with trapped red blood cells Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets Fibrin PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) Step 1: Vascular Spasms Step 2: Platelet Plug Formation Step 3: Coagulation +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 1 Step 1: Vascular Spasms

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  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  Platelets pile up to form a platelet plug

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 2 Injury to lining of vessel exposes collagen fibers; platelets adhere Collagen fibers Step 1: Vascular Spasms Step 2: Platelet Plug Formation

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 3 Injury to lining of vessel exposes collagen fibers; platelets adhere Platelet plug forms Collagen fibers Platelets Step 1: Vascular Spasms Step 2: Platelet Plug Formation

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 4 Injury to lining of vessel exposes collagen fibers; platelets adhere Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets PF 3 from platelets Calcium and other clotting factors in blood plasma Tissue factor in damaged tissue Step 1: Vascular Spasms Step 2: Platelet Plug Formation +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 5 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 6 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator ProthrombinThrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 7 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 8 Injury to lining of vessel exposes collagen fibers; platelets adhere Fibrin clot with trapped red blood cells Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets Fibrin PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) Step 1: Vascular Spasms Step 2: Platelet Plug Formation Step 3: Coagulation +

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Coagulation  Injured tissues release tissue factor (TF)  PF 3 (a phospholipid) interacts with TF, blood protein clotting factors, and calcium ions to trigger a clotting cascade  Prothrombin activator converts prothrombin to thrombin (an enzyme)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Coagulation (continued)  Thrombin joins fibrinogen proteins into hair- like molecules of insoluble fibrin  Fibrin forms a meshwork (the basis for a clot)

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.7

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Blood usually clots within 3 to 6 minutes  The clot remains as endothelium regenerates  The clot is broken down after tissue repair

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Undesirable Clotting  Thrombus  A clot in an unbroken blood vessel  Can be deadly in areas like the heart  Embolus  A thrombus that breaks away and floats freely in the bloodstream  Can later clog vessels in critical areas such as the brain

Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Bleeding Disorders  Thrombocytopenia  Platelet deficiency  Even normal movements can cause bleeding from small blood vessels that require platelets for clotting  Hemophilia  Hereditary bleeding disorder  Normal clotting factors are missing