1. Hematopoiesis
Blood cell formation Occurs in red bone marrow Adult red marrow is found in ribs, vertebrae, sternum, pelvis, proximal humeri, and proximal femurs.

2. Hematopoiesis
All blood cells are derived from a common stem cell (hemocytoblast)
Hemocytoblast differentiation
Lymphoid stem lymphocytes
Myeloid stem cell all other formed elements
Figure 10.4

3. Formation of Erythrocytes
Mature RBC are anucleate= NO NUCLEUS. Therefore, Unable to divide, grow, or synthesize proteins Wear out in 100 to 120 days When worn out, RBCs are eliminated by phagocytes in the spleen or liver Lost cells are replaced by division of hemocytoblasts in the red bone marrow

4. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Increased O2- carrying ability of blood
Erythropoietin stimulates
Kidney releases erythropoietin
Enhanced erythropoiesis
Red bone marrow
More RBCs
Normal blood oxygen levels
Imbalance
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
Figure 10.5

5. Control of Erythrocyte Production
Normal blood oxygen levels
Figure 10.5, step 1

6. Control of Erythrocyte Production
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Normal blood oxygen levels
Imbalance
Figure 10.5, step 2

7. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Normal blood oxygen levels
Imbalance
Figure 10.5, step 3

8. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Kidney releases erythropoietin
Normal blood oxygen levels
Imbalance
Figure 10.5, step 4

9. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Erythropoietin stimulates
Kidney releases erythropoietin
Red bone marrow
Normal blood oxygen levels
Imbalance
Figure 10.5, step 5

10. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Erythropoietin stimulates
Kidney releases erythropoietin
Enhanced erythropoiesis
Red bone marrow
More RBCs
Normal blood oxygen levels
Imbalance
Figure 10.5, step 6

11. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Increased O2- carrying ability of blood
Erythropoietin stimulates
Kidney releases erythropoietin
Enhanced erythropoiesis
Red bone marrow
More RBCs
Normal blood oxygen levels
Figure 10.5, step 7

12. Control of Erythrocyte Production
Reduced O2 levels in blood
Stimulus: Decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2
Increased O2- carrying ability of blood
Erythropoietin stimulates
Kidney releases erythropoietin
Enhanced erythropoiesis
Red bone marrow
More RBCs
Normal blood oxygen levels
Imbalance
Figure 10.5, step 8

13. Formation of White Blood Cells
Colony stimulating factors (CSFs) and interleukins prompt bone marrow to generate leukocytes

14. Formation of Platelets
The stem cell (megakaryocyte) undergoes mitosis without cytokinesis many times, forming a large, multinuclear cell, which then fragments into platelets.

15. Hemostasis
Stoppage of bleeding resulting from a break in a blood vessel
Hemostasis involves three phases
Vascular spasms
Platelet plug formation
Coagulation (blood clotting)

16. Hemostasis
Figure 10.6

17. Hemostasis- STEP 1 Vascular spasms
Vasoconstriction causes blood vessel to spasm
Spasms narrow the blood vessel, decreasing blood loss
Figure 10.6, step 1

18. Hemostasis- Step 2 Platelet plug formation
Injury to lining of vessel exposes collagen fibers; platelets adhere
Collagen fibers
Step 1: Vascular Spasms
Step 2: Platelet Plug Formation
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
Figure 10.6, step 2

19. Hemostasis – step 3 Coagulation
Injured tissues release tissue factor (TF)
PF3 (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)
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
PF3 from platelets
Calcium and other clotting factors in blood plasma
Tissue factor in damaged tissue
Step 1: Vascular Spasms
Step 2: Platelet Plug Formation +
Figure 10.6, step 4

20. Hemostasis – coagulation continued
Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky
PF3 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) +
Thrombin joins fibrinogen proteins into hair-like molecules of insoluble fibrin
Fibrin forms a meshwork (the basis for a clot)
Figure 10.6, step 7

21. Hemostasis
Blood usually clots within 3 to 6 minutes The clot remains as endothelium regenerates The clot is broken down after tissue repair
Figure 10.7

22. Summary of hemostasis
Hemostasis is initiated by a break in the blood vessel wall (or lining), initiating vascular spasms and causing platelets to cling to the damaged site. Once attached, the platelets release serotonin, which enhances vasoconstriction. Injured tissue cells release tissue factor, which interacts with platelet phospholipids (PF3), Ca2+ and plasma clotting factors to form prothrombin activator. Prothrombin activator converts prothrombin to thrombin. Thrombin, an enzyme, then converts soluble fibrinogen molecules into long fibrin threads, which form the basis of the clot and then traps erythrocytes flowing by in the blood.

23. Undesirable Clotting Coagulation can be promoted by:
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
Coagulation can be promoted by:
i. Roughened vessel lining, which attracts/activates platelets.
ii. Pooling of blood within vessels can result in the activation of clotting factors and the initiation of the coagulation process.

24. Bleeding Disorders Thrombocytopenia Platelet deficiency
Even normal movements can cause bleeding from small blood vessels that require platelets for clotting
The liver is the source of fibrinogen and several other factors that are necessary for clotting. When the liver is damaged and dysfunctional, it becomes unable to synthesize the usual amounts of clotting factors. When this situation happens, abnormal and often severe bleeding episodes can occur
Hemophilia
Hereditary bleeding disorder
Normal clotting factors are missing

25. The Royal Disease

26. Review Questions #1
What is the name of the stem cell that gives rise to all other formed elements?
Name the formed elements that arise from myeloid stem cells. Name those arising from lymphoid stem cells.
What property of RBCs dooms them to a limited life span of only 120 days?
What WBC type resides primarily in the tissues of the body?
How is the production of platelets different from that of all other formed elements?
Describe the process of hemostasis. Indicate what starts the process.
What factors enhance the risk of thrombus formation in intact blood vessels?
How can liver dysfunction cause bleeding disorders?

27. Blood Groups and Transfusions
Large losses of blood have serious consequences
Loss of 15–30% causes weakness
Loss of over 30% causes shock, which can be fatal
Transfusions are the only way to replace blood quickly
Transfused blood must be of the same blood group

28. Human Blood Groups
Blood contains genetically determined proteins Antigens (a substance the body recognizes as foreign) may be attacked by the immune system Antibodies are the “recognizers” Blood is “typed” by using antibodies that will cause blood with certain proteins to clump (agglutination)

29. Human Blood Groups
There are over 30 common red blood cell antigens The most vigorous transfusion reactions are caused by ABO and Rh blood group antigens

30. ABO Blood Groups Based on the presence or absence of two antigens
Type A
Type B
The lack of these antigens is called type O

31. ABO Blood Groups
The presence of both antigens A and B is called type AB The presence of antigen A is called type A The presence of antigen B is called type B The lack of both antigens A and B is called type O

32. ABO Blood Groups Blood type AB can receive A, B, AB, and O blood
Universal recipient
Blood type B can receive B and O blood
Blood type A can receive A and O blood
Blood type O can receive O blood
Universal donor

33. ABO Blood Groups
Table 10.3

34. Rh Blood Groups Rh+ Rh- O 38.5% 6.5% A 34.3% 5.7% B 8.6% 1.4% AB 4.3%
Named because of the presence or absence of one of eight Rh antigens (agglutinogen D) that was originally defined in Rhesus monkeys Most Americans are Rh+ (Rh positive) Problems can occur in mixing Rh+ blood into a body with Rh– (Rh negative) blood Percentage of Population with Each Blood Type
Rh+
Rh- O
38.5%
6.5% A
34.3%
5.7% B
 8.6%
1.4% AB
 4.3%
0.7%

35. Rh Dangers During Pregnancy
Danger occurs only when the mother is Rh– and the father is Rh+, and the child inherits the Rh+ factor RhoGAM shot can prevent buildup of anti-Rh+ antibodies in mother’s blood

36. Rh Dangers During Pregnancy
The mismatch of an Rh– mother carrying an Rh+ baby can cause problems for the unborn child
The first pregnancy usually proceeds without problems
The immune system is sensitized after the first pregnancy
In a second pregnancy, the mother’s immune system produces antibodies to attack the Rh+ blood (hemolytic disease of the newborn)

37. Blood Typing
Blood samples are mixed with anti- A and anti-B serum Coagulation or no coagulation leads to determining blood type Typing for ABO and Rh factors is done in the same manner Cross matching—testing for agglutination of donor RBCs by the recipient’s serum, and vice versa
Figure 10.8

38. Review Questions #2
What are the classes of human blood groups based on?
What are agglutinins?
Name the four ABO blood groups.
What is a transfusion reaction? Why does it happen?
10. What is the probable result from infusion of mismatched blood?
11. Cary is bleeding profusely after being hit by a truck as he was pedaling his bike home. At the hospital, the nurse asked him whether he knew his blood type. He told her he “had the same blood as most other people.” What is his ABO blood type?
What is the difference between an antigen and an antibody?
Explain why a Rh- person does not have a transfusion reaction on the first exposure to Rh+ blood? Why is there a transfusion reaction the second time he or she receives the Rh+ blood?