1. The Human Body in Health and Illness, 4th edition
Barbara Herlihy
Chapter 15:
Blood

2. Lesson 15-1 Objectives Describe the three functions of blood.
Describe the composition of blood.
Describe the three types of blood cells: erythrocytes, leukocytes, and thrombocytes.
Explain the formation of blood cells.
Explain the breakdown of red blood cells and the formation of bilirubin.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

3. Three General Functions of Blood
Transportation
Oxygen, nutrients, waste
Regulation
Temperature, acid-base, fluid-electrolyte balance
Protection
Against infection and bleeding
What happens to tissue if it is deprived of oxygen?
Tissue dies (suffers necrosis) when deprived of oxygen.
How do vasodilation and vasoconstriction affect temperature?
Vasodilation brings blood to the surface and allows heat to dissipate, whereas vasoconstriction shunts blood to the core of the body and preserves heat.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

4. Hematocrit Plasma the colorless fluid part of blood Formed elements
55% of total
Clear yellowish liquid
Formed elements
45% of total
Erythrocytes (RBCs)
Leukocytes (WBCs)
Thrombocytes (platelets)
The hematocrit is the percentage of formed cells in a sample of blood. The two parts of the blood are illustrated in this test tube. The two phases appear after the blood is collected and spun in a tube. The buffy coat is the thin layer of cells between the plasma and the RBCs. It consists of WBCs and platelets.
Why may the hematocrit of a dehydrated person be falsely elevated?
Because hematocrit is a ratio, a decline in plasma falsely elevates the percentage of formed elements.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

5. Hemopoiesis Process of blood cell production
Two locations of hemopoiesis
Myeloid hemopoiesis in red bone marrow
Lymphoid hemopoiesis in lymphoid tissue
Hemopoiesis consists of the production of red blood cells (erythropoiesis), the production of white blood cells (leukopoiesis), and the production of platelets (thrombopoiesis).
Myeloid hemopoiesis produces RBCs, WBCs, and platelets. Lymphoid tissues produces only lymphocytes, a type of WBC.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

6. Bone Marrow Depression
Occurs if bone marrow cannot produce enough blood cells.
Also called myelosuppression
Results
Aplastic anemia: RBC deficiency
Leukopenia: WBC deficiency
Thrombocytopenia: Platelet deficiency
Pancytopenia: Depression of all blood cells
Many drugs and certain procedures, such as radiation therapy, depress the bone marrow; therefore, a person exposed to any of these therapies must be monitored for symptoms of myelosuppression.
A person with leukopenia is susceptible to infection, and a person with thrombocytopenia is at high risk for hemorrhage.
Some drugs stimulate the bone marrow, thereby relieving the symptoms of myelosuppression.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

7. Overactive Bone Marrow
Overactive bone marrow leads to excess RBC production.
Called polycythemia (vera or secondary)
Polycythemia vera
Burdens the heart
Overwhelms clotting system
Causes beet-red face and palms
A person with polycythemia vera, or excess RBCs, may be given a drug to depress bone marrow or undergo a phlebotomy to remove excess blood.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

8. Red Blood Cells: Oxygen Carriers
Large, disc-shaped
Bendable
Contain hemoglobin
Globin shapes RBC
Heme carries iron
Iron carries O2
Each globin chain carries a heme.
O2 binds loosely to the iron in the hemoglobin so the O2 is easily released at the tissue level.
If the globin is misshapen, the RBC will be misshapen, as in sickle cell anemia.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

9. Why Blood Changes Its Color
Oxyhemoglobin
O2 binds loosely with iron (Fe)
Makes blood bright red
Lack of O2 makes blood bluish red
Carbon monoxide (CO) binds to the iron site, like oxygen, causing blood to become cherry red.
Why does CO poisoning make the patient hypoxemic but not cyanotic?
CO binds to iron, which makes the blood bright red, but it prevents the carrying of oxygen.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

10. Shape of Red Blood Cells
Large disc, thick rim
RBC bends, fits through tiny vessels to deliver O2
Sickle cell anemia: RBC does not bend, blocks vessel, fails to deliver O2
It is important that the RBC be able to bend so that it can fit through the capillaries. Misshapen globin prevents this proper bending.
Why do sickled RBCs cause organ damage and pain, as in part C of the illustration?
The sickled RBC blocks the flow of blood through the capillaries, thereby depriving the cells of oxygen and nutrients.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

11. Rapid breakdown of RBCs
Jaundice
Hemolytic Jaundice
Rapid breakdown of RBCs
Hyperbilirubinemia
Yellow stained tissue
Obstructive Jaundice
Normal rate of RBC breakdown but diminished excretion of bilirubin in bile
Yellow, stained tissue
Hyperbilirubinemia causes jaundice. It develops if there is an excess production of bilirubin, as in hemolysis, or diminished excretion, as in hepatobiliary disorders.
Why does a stone in the common bile duct cause jaundice?
The stone blocks the excretion of bilirubin in the bile, causing hyperbilirubinemia and jaundice.
How would the jaundice resulting from a bile duct obstruction be relieved?
Removal of the stone will relieve the jaundice.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

12. Anemia: Insufficient RBCs
RBC production falters if conditions are disordered or necessary substances are missing.
The absence of iron, vitamin B12, and folic acid causes anemia.
A healthy bone marrow, genetic code, and functioning kidneys (erythropoietin) are necessary for RBC production.
Rapid hemolysis can also cause anemia.
Why is the little yellow baby shown in the anemia slide?
She has excess hemolysis, hyperbilirubinemia, and jaundice. The hemolysis decreases her RBC count. This condition is often seen in neonates.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

13. White Blood Cells (WBCs)
Protect the body against infection and inflammation
Phagocytes
Neutrophils
Monocytes
Can leave the blood vessels
To site of infection or inflammation
Leukocytosis is excess WBCs, a response to infection and inflammation.
Leukopenia is a deficiency of WBCs. It is usually caused by myelosuppression.
A few infections are characterized by leukopenia rather than leukocytosis.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

14. Lesson 15-2 Objectives Identify the steps of hemostasis.
Describe the four blood types.
Describe the Rh factor.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

15. Hemostasis: Stopping Bleeding
Vascular spasm
Platelet plug
Coagulation
The smooth muscle in a blood vessel wall responds to injury by contracting. This is called vascular spasm. When torn, the inner lining of a blood vessel activates the platelets. Both the injured vascular lining and platelets become sticky, forming a platelet plug.
Why would a large crush injury to a finger often cause less bleeding than a paper cut?
The crush injury causes more vascular spasm.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

16. Formation of a Blood Clot
Injury produces PTA.
PTA activates prothrombin to form thrombin.
Thrombin activates fibrinogen to form fibrin fibers (clot).
Clot retraction
The injured vascular wall and the activated platelets stimulate the coagulation factors, resulting in a fibrin clot.
Clots retract to squeeze water out of the clot. This pulls the edges of the injured vessel together to facilitate healing.
Explain the different mechanisms whereby the anticoagulants Coumadin (C) and heparin (H) work?
Coumadin interferes with the uptake of vitamin K in the hepatic synthesis of prothrombin. Heparin is an antithrombin agent.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

17. Fibrinolysis: Clot Breakdown
After the clot has done its job, it needs to be dissolved.
Tissue plasminogen activator (TPA) is formed by injured tissue. Plasmin dissolves the clot.
When administered as a drug, TPA is called a clot buster. It can prevent the tissue damage that a clot may cause in a heart attack or stroke. This is true only if the heart attack or stroke was caused by a clot. If the cause was a hemorrhage, administration of TPA will increase the bleeding.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

18. Drugs that Affect Clotting
Antiplatelet drugs
Aspirin, NSAIDs, clopidogrel
Anticoagulants
Heparin (antithrombin)
Coumadin (prevents formation of prothrombin)
Fibrinolytic or “clot buster” drugs
Tissue plasminogen activator (TPA)
Why are patients with heart disease advised to take low-dose aspirin each day?
Aspirin therapy helps prevent clot formation.
Why is vitamin K the antidote to Coumadin?
Coumadin blocks the use of vitamin K in the hepatic synthesis of prothrombin.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

19. Four Types of Blood Type A  A antigen on RBC
 Anti-B antibodies in plasma
Type B
 B antigen on RBC
 Anti-A antibodies in plasma
Blood is classified according to specific antigens on the surface of the RBC. There are two classification systems, by ABO group and by Rh factor (not listed here).
Type A blood has the A antigen. What would happen if the plasma had anti-A antibodies?
The anti-A antibodies would attack the A antigen, cause clumping within the blood.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

20. Four Types of Blood (cont’d.)
Type AB
 Both A and B antigens on RBC
 Neither anti-A nor anti-B antibodies in plasma
Type O
 Neither A nor B antigen on RBC
 Both anti-A and anti-B antibodies in plasma
Why are there neither anti-A nor anti-B antibodies in the plasma of type AB blood?
The anti-A and anti-B antibodies would agglutinate the A and B antigens on the surface of the RBC.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

21. Agglutination: Clumping of RBCs
Blood clumps in response to interactions between antigens and antibodies.
Example of a mismatched transfusion
Type A recipient has A antigens on RBC and anti-B antibodies in plasma
 Type B donor has B antigen on RBC
 Result: Anti-B antibodies of recipient attack B antigen of donor’s blood, causing agglutination and hemolysis.
In another case, the recipient is type B and the donor is type A. Why does this represent an incompatible blood transfusion?
The anti-A antibodies of the recipient attack the A antigen of the donor.
Why does mismatched blood cause hemolysis?
The agglutination destroys the RBCs. Agglutination also adversely affects many organs, particularly the kidney This can be fatal.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

22. Type O: “Universal” Blood Donor
Type O blood has no antigens on RBCs.
Anti-A and anti-B antibodies of all other blood types have no antigen to attack.
So, type O blood can be safely donated to all recipients.
In the event of mass disaster, why is donor type O blood so valuable?
Type O blood contains neither A nor B antigens, so it can be administered to people with type A, B, AB, or O blood.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

23. Type AB: “Universal” Recipient
Type AB has neither anti-A nor anti-B antibodies in the plasma.
Type AB has no antibodies to attack antigens in any blood type—A, B, AB, or O.
So, type AB can safely receive blood of any type.
Explain why a type AB recipient can receive type A donor blood.
The blood of the AB recipient contains no anti-A antibodies.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

24. Rh Factor: An Additional Antigen
People with Rh factor are Rh positive (+).
 Types A(+), B(+), AB(+), and O(+)
Those without Rh factor are Rh()
 Types A(), B(), AB(), and O()
Rh() persons initially have no anti-Rh antibodies in their blood, but develop them after exposure to the Rh factor.
Blood is said to be Rh-positive if an RBC has the Rh factor. It is said to be Rh-negative if it lacks the Rh factor.
Plasma does not naturally carry anti-Rh antibodies; however, the plasma of an Rh-negative person can develop anti-Rh antibodies from receiving Rh-positive blood and becoming sensitized.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

25. Rh Factor: Two Considerations
Blood transfusions
 Rh() blood can be donated to Rh(+) recipients
 Rh(+) blood cannot be donated to Rh() recipients
The true universal donor is O().
The true universal recipient is AB(+).
Rh incompatibility during pregnancy causes erythroblastosis fetalis.
If the universal donor is type O, why can type O(+) not be given to a person who is A()?
The recipient will produce anti-Rh antibodies, causing agglutination. Type O(+) cannot be given to A(), B(), AB(), and O(). Therefore, the true universal donor is type O(-).
Type AB() cannot receive any Rh-positive blood. Type AB(+), however, can receive both Rh(+) and Rh(-) blood. It is therefore the true universal recipient.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

26. Rh Incompatibility in Pregnancy
Condition: Mother is Rh() and baby is Rh(+).
In late pregnancy, Rh(+) blood moves from baby to mother.
Mother develops anti-Rh antibodies.
Mother’s anti-Rh antibodies move into baby, causing agglutination and hemolysis.
Usually the first Rh(+) baby will not suffer agglutination and jaundice, because the mother has not developed enough anti-Rh antibodies.
If the mother becomes pregnant again with an Rh(+) fetus, the baby will develop a condition called erythroblastosis fetalis as the mother’s anti-Rh antibodies attack the baby’s RBCs. Death of the fetus or severe mental retardation can result.
Erythroblastosis fetalis can be prevented by the administration of a drug called RhoGAM. When administered to the mother, the drug makes the baby’s RBCs nonantigenic. This is illustrated on the next slide.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.

27. Erythroblastosis Fetalis
Using the diagram on the slide, predict what would happen if both the mother and the child had type A() blood.
Because the baby’s RBCs have no Rh factor, they do not stimulate the production anti-Rh antibodies in the mother. Therefore, there is no possibility of erythroblastosis fetalis.
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved.