CHAPTER 14: BLOOD

Topical Chapter Outline

14.1 Introduction
14.2 Blood Cells
a. The Origin of Blood Cells
b. Characteristics of Red Blood Cells
c. Red Blood Cell Counts
d. Red Blood Cell Production and Its Control
e. Dietary Factors Affecting Red Blood Cell Production
f. Destruction of Red Blood Cells
g. Types of White Blood Cells
h. Functions of White Blood Cells
i. White Blood Cell Counts
j. Blood Platelets
14.3 Blood Plasma
a. Plasma Proteins
b. Gases and Nutrients
c. Nonprotein Nitrogenous Substances
d. Plasma Electrolytes
14.4 Hemostasis
a. Blood Vessel Spasm
b. Platelet Plug Formation
c. Blood Coagulation (Extrinsic Clotting Mechanism, Intrinsic Clotting
Mechanism, and Fate of Blood Clots)
d. Prevention of Coagulation
14.5 Blood Groups and Transfusions
a. Antigens and Antibodies
b. ABO Blood Group
c. Rh Blood Group

LEARNING OUTCOMES:
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 CHAPTER 14: BLOOD

14.1 Introduction

1. Describe the general characteristics of blood, and discuss its major functions.

2. Distinguish among the formed elements of blood and the liquid portion of blood.

14.2 Blood Cells

3. Describe the origin of blood cells.

4. Explain the significance of red blood cell counts and how they are used to
diagnose disease.

5. Discuss the life cycle of a red blood cell.

6. Summarize the control of red blood cell production.

7. Distinguish among the five types of white blood cells and give the function(s) of
each type.

8. Describe a blood platelet, and explain its functions.

14.3 Blood Plasma

9. Describe the functions of each of the major components of plasma.

14.4 Hemostasis

10. Define hemostasis, and explain the mechanisms that help to achieve it.

11. Review the major steps in coagulation.

12. Explain how to prevent coagulation.

14.5 Blood Groups and Transfusions

13. Explain blood typing and how it is used to avoid adverse reactions following
blood transfusions.

14. Describe how blood reactions may occur between fetal and maternal tissues.

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 CHAPTER 14: BLOOD
14.1 INTRODUCTION

A. Blood is a type of connective tissue whose cells are suspended in a liquid

extracellular matrix, called plasma.
B. Blood transports substances between body cells and the external
environment and helps maintain a stable internal environment.
C. Blood volume varies with body size, fluid and electrolyte balance, and
adipose content.
1. Average blood volume (70 kg male) is 5 liters.
D. Blood can be separated into two major components:
See Fig 14.1-14.3, page 524.

1. Blood cells or "formed elements" (45% by weight), which is composed

mainly of red blood cells.
a. Quantitative analysis of this portion of blood represents the
hematocrit (HCT) reading or packed cell volume (PCV).
2. Plasma (55% by weight), liquid portion that contains
including water, proteins, amino acids, carbohydrates, lipids, vitamins,
hormones, electrolytes, and cellular wastes.

14.2 BLOOD CELLS (or “formed elements”)

Blood is composed of three types of cells, including erythrocytes (red blood cells),
leukocytes (white blood cells), and thrombocytes (platelets).

See Fig 14.1, page 524.

A. The Origin of Blood Cells

1. Hematopoietic stem cells in red bone marrow of adults

o Yolk sac, liver, and spleen in fetuses

2. Specific types of hematopoietic growth factors produce differentiation

resulting in specific types of cells.
o Myeloid stem cells
o Lymphoid stem cells

3. ALL BLOOD CELLS ARE FORMED FROM THE SAME LARGE

PRIMITIVE CELL CALLED A HEMOCYTOBLAST .

See Fig 14.4, page 525

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 CHAPTER 14: BLOOD
14.2. BLOOD CELLS

B. Erythrocytes (Red Blood Cells)

1. Characteristics of Red Blood Cells (RBC) = Erythrocytes

See Fig 14.5, page 526.
a. tiny, 7.5m diameter, biconcave disks (increased surface area)
b. compose 99% of blood cells
c. contain hemoglobin, which is loosely bound to oxygen.
See Fig 14.9, page 531.
o Hemoglobin = protein (globin) + heme (iron)
o oxyhemoglobin = bright red
o deoxyhemoglobin = darker red, purple
* See box on page 527 re: Sickle Cell Disease.
* See Clinical Application 14.1, page 530, re: King
George III and Porphyria Variegata.
d. Mature cells lack nuclei (i.e. are anucleate), leaving more
room for hemoglobin and oxygen.

2. Red Blood Cell Counts

a. RBC Count (RCC) = the number of RBC's/mm3 blood.
o Average RCC = 4 million-6 million RBC's/mm3
blood (in a healthy individual).

3. Red Blood Cell Production and Its Control

a. Production (Erythropoiesis)
o In fetuses = yolk sac, liver, spleen
o In adults = red bone marrow
b. Control of Production
RBC number remains
relatively stable.
o Negative feedback
mechanism involving the hormone erythropoietin, which
is produced and secreted by the special cells in the kidney
and liver.
o See Fig 14.6, page 528.
1. Chemoreceptors in kidney and liver detect
low blood oxygen.
2. Erythropoietin is released from kidney and
liver into circulation.
3. Erythropoietin
targets red bone marrow (in epiphyses of long
bones and spongy bone of flat bones), stimulating
erythropoiesis.

4. Dietary Factors Affecting RBC Production

a. B12, folic acid, and iron are all needed.

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 CHAPTER 14: BLOOD
b. Intrinsic Factor is secreted by stomach allowing B12 absorption.
c. Lack of proper nutrients leads to anemia (see below).
* See Table 14.1 and box on page 529.

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14.2. BLOOD CELLS

B. Erythrocytes (Red Blood Cells)

5. Destruction of RBCs
Average life-span = 120 days
a. Liver and spleen macrophages destroy worn RBCs.
b. Hemoglobin is broken into globin and heme.
c. Iron in Hb is recycled.
d. Heme is broken into biliverdin > bilirubin > bile.
e. See Table 14.3, page 531 and Fig 14.7, page 528.

* See Table 14.2 and Fig 14.8, page 529, Types of Anemias.

C. Leukocytes (White Blood Cells)

1. Types and Function of WBCs

There are five types of leukocytes that function to control disease.

Leukocytes are divided into granulocytes and
agranulocytes:

a. Granulocytes (are approximately 12-14µ in diameter).

1. Neutrophils: See Figures 14.10,

page 532.
 most abundant WBC = 54%-62%
 polymorphonucleocyte (PMN)
 phagocytosis of foreign particles (disease
organisms & debris)
 increased in acute bacterial infections
2. Eosinophils: See Figures 14.11, pages 532.
 1-3% of total WBC
 kill parasites and are responsible for allergic
reactions
 increased during parasitic infections (tapeworm,
hookworm)
 release histamine during allergic reactions
3. Basophils: See Figures 14.12, page 532.
 <1% of total WBC
 release heparin which inhibits blood clotting
 release histamine, a vasodilator helpful
inflammatory responses (increases blood flow to
damaged tissue).
 may leave bloodstream and develop into mast cells
(antibodies attach and cause mast cell to burst,
releasing allergy mediators. Discussed in greater
detail in Chapter 16.)
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14.2 BLOOD CELLS

C. Leukocytes (White Blood Cells)

1. Types and Function of WBC’s
b. Agranulocytes
1. Monocytes: See Fig 14.13, page 532.
 3-9% of total WBC
 phagocytosis
 largest WBC, 12-20 µ in diameter
 In blood = phagocyte. In tissues = macrophage.
 increased during typhoid fever, malaria, and
mononucleosis
2. Lymphocytes: See Fig 14.14, page 533.
 5-33% of total WBC
 live for several months to years (only leukocyte that
lives more than a few days)
 smallest WBC, ranging in size from large (10-14)
to small (6-9)
 function in immunity
 Discussed in greater detail in Chapter 16.
 increased during TB, whooping cough, viral
infections, tissue rejection reactions, and tumors

2. Diapedesis = process by which leukocytes move through blood vessel

walls to enter tissues.
a. Monocyte to macrophage
b. Basophil to mast cell
See Fig 14.15, page 533.

3. WBC Counts
a. Average WBC count (WCC) = 5000-10,000 WBC’s / mm3 blood
1. Number of WBC’s increases during infections
o leukocytosis = WCC > 10000
o leukopenia = WCC < 5000
b. Differential white blood cell count (DIFF) indicates % of
each particular leukocyte.
c. Leukemia = abnormal (uncontrolled) production of
specific types of immature leukocytes. See Clinical Application
14.2, pages 535-536.
D. Thrombocytes (Blood Platelets)
1. fragments of giant cells called megakaryocytes
2. Normal count = 130,000-360000 platelets/ mm3 blood.
3. Function = blood clotting (will be discussed in more detail later).

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 CHAPTER 14: BLOOD
14.2. BLOOD CELLS

Major Blood Cell Summary Table (See Summary of Blood Cells in Table 14.5, page 536

Major Blood Cell

Type

Scientific Name

Circulating
Concentration/
mm3 blood

General Function

Key Characteristics

White Blood Cell Summary Table

Specific WBC Function/ Differential % Typical Sketch

Event of Increase?

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14.3 BLOOD PLASMA See Fig 14.1-Fig 14.3, page 524.
Blood plasma is clear, yellow liquid, composed of water,
proteins, nutrients, gases, electrolytes, and many more
substances.
A. WATER:
1. 92 %
2. functions as solvent, in transport, temperature regulation, and serves as
site of metabolic reactions
B. Plasma Proteins: See Table 14.6, page 537.
1. 7% of plasma volume
2. all produced in the liver
3. Three types:
a. albumin
o maintains osmotic pressure of cells (0.9%)
o transports fatty acids
b. globulins ( α, β , γ )
o antibodies
c. fibrinogen
o blood clotting

C. Plasma Gases:
1. oxygen (needed for cellular respiration)
2. carbon dioxide (produced by cell respiration)
3. nitrogen (use unknown)

D. Plasma Nutrients:
1. amino acids
2. monosaccharides (i.e. glucose)

E. Nonprotein Nitrogenous Substances (Plasma Wastes):

1. urea (amino acid metabolism),
2. uric acid (nucleotide metabolism)
3. creatinine (creatine metabolism)
4. creatine (CP to recycle ADP to ATP in muscle & brain)
5. bilirubin (hemoglobin metabolism)

F. Plasma Electrolytes:
1. includes sodium, potassium, calcium, magnesium, chloride,
bicarbonate, phosphate, and sulfate
2. Maintain osmotic pressure, resting membrane potential, and pH.

G. Regulatory Substances:
1. enzymes
2. hormones

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 CHAPTER 14: BLOOD
14.4 HEMOSTASIS

A. Definition: Hemostasis = stoppage of bleeding from a blood vessel.

B. 3 steps involved: See Table 14.7, page 539.

1. Blood Vessel Spasm (vessel walls constrict)

a. vasospasm
b. reduces blood flow

2. Platelet Plug Formation See Fig 14.17, page 538.

a. Platelets become sticky and adhere to one another.
b. Platelets also release the hormone serotonin, which causes further
vasoconstriction of the vessel.

3. Blood Coagulation = formation of a blood clot

a. complex cascade of events (positive feedback mechanism)
b. requires calcium ions
c. 2 possible starting pathways
o Extrinsic Clotting Mechanism
1. Starts when platelet contacts damaged tissue or
tissue outside of blood vessel (hence, extrinsic)
2. Cascade leads to prothrombin activator (PA) release
by platelets
3. PA and Ca2+ cause prothrombin to convert to
thrombin
4. Thrombin catalyzes the final step, (polymerization
of) fibrinogen to fibrin.
5. Fibrin threads make up meshwork of clot.
o Intrinsic Clotting Mechanism (all factors normally found
in blood)
1. Starts when blood contacts a foreign substance
2. Cascade again leads to same final steps as above.
a. Final step = fibrinogen → fibrin.
d. Fate of Blood Clots
○ A formed clot retracts and pulls the edges of a
broken blood vessel together.
1. A thrombus is an abnormal blood clot in a
vessel.
2. An embolus is a clot or fragment of
a clot that moves in a vessel.
○ Fibroblasts invade a clot, forming connective tissue
throughout.
○ Protein-splitting enzymes may eventually destroy a
clot.

e. See scanning electron micrograph, Fig 14.18, page 539.

f. See Fig 14.19, page 540 and Tables 14.8 and 14.9, page 541.

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 CHAPTER 14: BLOOD
14.4 HEMOSTASIS

C. Prevention of Coagulation (Fibrinolytic System)

1. Fibrinolytic system provides checks and balances so that blood clotting

does not go awry.

2. See Table 14.10, page 543 re: Factors That Inhibit Blood Clot Formation.

3. Definitions:
a. Thrombus = abnormal clot.
b. Embolus = floating clot (abnormal).
c. Embolism = when embolus gets lodged in a small vessel
obstructing blood flow.

4. Fibrinolytic substances include:

a. tissue plasminogen activator (TPA):

o naturally produced
o Also injected quickly after MI to dissolve coronary
thrombus(i).
o See box on page 542.

b. Heparin is an anticoagulant:

o naturally produced by basophils and mast cells

o Also used a pharmacologic agent extracted from lung
tissues of animals
 used during open-heart surgery and hemodialysis
 used immediately following
thrombus detection (i.e deep vein thrombosis, DVT,
see below)

c. Warfarin (Coumadin) is another anticoagulant:

o given to patients prone to thrombosis

o slower acting than heparin

* See Fig 14.20, page 542 re: Atherosclerosis.

* See Clinical Application 14.3, page 543 re: Deep Vein Thrombosis
(DVT).

* See box on page 543 re: Medicinal Uses of the Leech.

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 CHAPTER 14: BLOOD
14.5 BLOOD GROUPS AND TRANSFUSIONS

A. Antigens and Antibodies

1. There are antigens present on the cell membrane surface of

our erythrocytes (red blood cells).

2. Our plasma contains substances called antibodies that are produced

against non-self antigens.

3. If the RBC antigen (donor) and plasma antibody (recipient) are the same,
the serious condition of hemolysis (bursting) of RBC will occur.

* In the laboratory, this situation can be simulated, however the result is

termed agglutination = clumping of red blood cells.
See Fig 14.22, page 545.

B. ABO Blood Group: See Fig 14.21, page 545 and Table 14.12, page 544.

1. inherited trait

2. determined by the antigens on a person's RBC

3. 4 types: A, B, AB, O
a. Type A blood = antigen A on RBC
b. Type B blood = antigen B on RBC
c. Type AB blood = both antigen A & B on RBC
d. Type O = neither A or B antigen on RBC

4. Antibodies in plasma: (See above figure)

a. Shortly after birth, we spontaneously

develop antibodies against RBC antigens that are not our own (i.e.
non-self).

b. Antibodies formed include:

o Persons with Type A blood, develop Anti-B antibodies
o Persons with Type B blood, develop Anti-A antibodies
o Persons with Type AB blood, do not develop either Anti-A
or Anti-B antibodies
o Persons with Type O blood, develop both Anti-A and Anti-
B antibodies.

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14.5 BLOOD GROUPS AND TRANSFUSIONS

C. Summary of ABO Interactions:

When considering blood transfusion reactions, the most important factor to

consider is the antibodies present in the recipient's plasma!

BLOOD TYPE

ANTIGEN ON
RBC

ANTIBODIES IN
PLASMA

COMPATIBLE
DONORS

INCOMPATIBLE
DONORS

GENOTYPE

PHENOTYPE

* A person with type O blood is considered the universal donor.

* A person with type AB blood is considered the universal recipient.

* See Table 14.11, page 544 re: ABO Blood Type Frequencies (%) within the United
States.

* See From Science to Technology 14.1, page 546 re: Blood Typing and Matching: From
Serology to DNA Chips.

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14.5 BLOOD GROUPS AND TRANSFUSIONS

D. Rh Blood Group:

1. inherited trait

2. studied in rhesus monkeys (thus, Rh)

3. Group of antigens present on RBC = Rh positive;

Lack of antigens on RBC = Rh negative.

4. Rh antibodies do not form spontaneously, but will form in Rh-negative

persons in response to stimulation:

a. Initial exposure (transfusion, etc.) does not produce harmful

effects, however the Rh-negative person has now been sensitized
(i.e. they can produce anti-Rh antibodies)

b. Additional exposure (transfusion, etc.) causes serious hemolysis to

occur.

5. Erythroblastosis fetalis = hemolytic disease of the newborn (HDN).

See Figure 14.23, page 547.

a. Scheme:

o Rh-negative mother becomes pregnant with Rh-positive

fetus.
o Pregnancy uneventful, but during birth, baby's blood enters
the mother's circulation and causes her to produce anti-Rh
antibodies.
o Mother conceives a second Rh-positive fetus.
o Mother's anti-Rh antibodies can now pass through the
placenta and enter the fetus’ circulation.
o The fetus’ RBC hemolyze resulting in this fatal condition.

b. Usually, no longer a significant problem because of the

administration of a drug called RhoGAM, which destroys the
mother's anti-Rh antibodies before they can cross the placenta and
destroy the fetus’ red blood cells.

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BLOOD DISORDERS

A. Sickle Cell Disease. See box on page 527.

B. Types of Anemias. See Table 14.2 and Fig 14.8, page 529.

C. King George III and Porphyria Variegata. See Clinical Application 14.1, page
530.

D. Leukemia. See Clinical Application 14.2, pages 535-536.

E. Edema. See box on page 537.

F. DIC, Disseminated intravascular clotting. See box on page 539.

G. Atherosclerosis. See Fig 14.20, page 542.

H. Thrombocytopenia. See box on page 542.

I. See Clinical Application 14.3, page 543 re: Deep Vein Thrombosis (DVT)

K. Some Inherited Disorders of Blood. See Table 14.14. page 548.

OTHER INTERESTING TOPICS:

A. Universal Precautions. See introduction on page 523.

B. See Table 14.11, page 544 re: ABO Blood Type Frequencies (%) within the
United States.

C. See From Science to Technology 14.1, page 546 re: Blood Typing and Matching:
From Serology to DNA Chips.

CHAPTER SUMMARY – see pages 548-550.

CHAPTER ASSESSMENTS – see pages 550-551

INTEGRATIVE ASSESSMENTS/ CRITICAL THINKING– see page 551.

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