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Essentials of Human Anatomy & Physiology

Thirteenth Edition
Global Edition

Chapter 10

Blood

Edited by ISD- Anatomy & Physiology


Faculty in November 2022

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Learning Outcomes
1. Describe the composition and volume of
whole blood.
2. Describe the composition of plasma, and
discuss its importance in the body.
3. List the cell types making up the formed
elements, and describe the major functions of
each.
4. Define anemia, polycythemia, leukocytosis,
leukopenia and leukemia, and list possible
causes for each condition.
Learning Outcomes
5. Explain the role of the hemocytoblast.
6. Describe the formation of red blood cells,
white blood cells and platelets.
7. Describe the blood-clotting process.
8. Discuss the disorders of hemostasis
(undesirable clotting and bleeding disorders).
9. Describe the ABO and Rh blood groups.
10.Explain the basis for a transfusion reaction.
Blood
• Blood transports everything that must be carried
from one place to another through blood vessels,
such as:
– Nutrients (glucose, fatty acids, amino acids)
– Vitamins
– Wastes (urea, uric acids)
– Hormones (such as thyroid hormones)
– Respiratory gases (O2 and CO2)
– Body heat

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Components of Blood
• Blood is the only fluid tissue, a type of
connective tissue, in the human body.

• Components of blood
1) Formed elements (living cells) such as
RBCS, WBCs and platelets.

2) Plasma (nonliving fluid matrix)

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• When blood is separated:
– Plasma rises to the top (55% of
blood).

– Erythrocytes, or red blood cells,


sink to the bottom (45% of blood, a
percentage known as the hematocrit
(hct))

– Buffy coat contains leukocytes, or


white blood cells, and platelets
(less than 1% of blood)
▪ Buffy coat: is a thin, whitish layer
between the erythrocytes and
plasma
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Figure 10.1
The
Composition
of Blood

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Blood: Physical Characteristics and Volume
– Sticky, opaque fluid
– Heavier and thicker than water
– Color range
▪ Oxygen-rich blood is scarlet (bright) red
▪ Oxygen-poor blood is dull (dark) red or purple
– Metallic, salty taste
– Blood pH is slightly alkaline, between 7.35 and 7.45
– Blood temperature is slightly higher than body
temperature, at 38⁰C.
• Blood volume about 5–6 liters of blood are found in a
healthy adult.
• Blood makes up 8% of body weight.
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Plasma
• 90% water
• Straw (pale yellow)-colored fluid
• Includes many dissolved substances:
– Nutrients (glucose, amino acids and fatty acids)
– Salts (electrolytes) such as Na+, K+ & Cl-
– Respiratory gases (O2 and CO2)
– Hormones (thyroid hormones)
– Plasma proteins (albumins, globulins and fibrinogens)
– Waste products (urea and uric acids)

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• Plasma proteins
– Most abundant solutes in plasma
– Most are made by the liver
– Include:
▪ Albumin—an important blood buffer and
contributes to osmotic pressure.

▪ Fibrinogens (clotting proteins)—help to


make a clot that stops blood loss when a blood
vessel is injured.

▪ Globulins —help in making antibodies that


protect the body from pathogens.
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Formed Elements

• Erythrocytes
– Red blood cells (RBCs)

• Leukocytes
– White blood cells (WBCs)

• Platelets
– Cell fragments

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Figure 10.2 Photomicrograph of a Blood Smear

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Erythrocytes (Red Blood Cells, or RBCs)

– Main function is to carry oxygen

– RBCs differ from other blood cells:


▪ Anucleate (no nucleus)
▪ Contain few organelles; lack mitochondria
▪ Make ATP by anaerobic means
▪ Essentially “bags” of hemoglobin (Hb)
▪ Shaped like biconcave discs

– Normal count is 5 million RBCs per cubic


millimeter (mm3) of blood.
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• Hemoglobin consists of four ribbon-like protein chains called
globins; bound to each globin is an iron-containing molecule
called heme.

• Each heme molecule can combine with one molecule of


oxygen; therefore, one hemoglobin molecule can unite with
four molecules of oxygen to form oxyhemoglobin.

• Hemoglobin also carries CO2, but instead of binding with


heme, CO2 binds with globin.

• How much oxygen the blood can carry depends on the


quantity of RBCs and hemoglobin it contains.

• Normal blood contains 12–18 grams of hemoglobin per 100


milliliters (m l) of blood
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Hemoglobin

Globins Heme

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• Homeostatic imbalance of RBCs
– Anemia is a decrease in the oxygen-carrying ability of
the blood due to:
▪ Lower-than-normal number of RBCs (hemorrhage)
▪ Abnormal or deficient hemoglobin content in the
RBCs (lack of iron in diet, prolonged bleeding such
heavy menstruation)
– Polycythemia
▪ Disorder resulting from excessive or abnormal
increase of RBCs due to:
– Bone marrow cancer (polycythemia vera)
– Life at higher altitudes (secondary polycythemia)
▪ Increase in RBCs slows blood flow and increases
blood viscosity (stickiness)
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– Sickle cell anemia (SCA)
results from abnormally
shaped hemoglobin

Homeostatic Imbalance 10.1


Comparison of (a) a Normal
Erythrocyte to (b) a Sickled
Erythrocyte
left parenthesis 6,550 times right parenthesis

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Leukocytes (White Blood Cells, or WBCs)
– Crucial in body’s defense against disease
– Complete cells, with nucleus and organelles.
– 4,800 to 10,800 WBCs per mm3 of blood.

– Respond to chemicals released by damaged


tissues (known as positive chemotaxis).

– Able to move into and out of blood vessels


(via diapedesis). Move by amoeboid motion
by forming cytoplasmic extensions to help
them move.
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• Homeostatic imbalance of WBC s
– Leukocytosis
▪ Is a condition in which the total WBC count is more
than 11000 cells /mm3 . It could be a normal
response to an infection or could be due to
excessive production of abnormal WBCs as in
leukemia.
– Leukopenia
▪ Abnormally low WBC count
▪ Commonly caused by certain drugs, such as
corticosteroids and anticancer agents
– Leukemia
▪ Bone marrow becomes cancerous
▪ Numerous immature WBC are produced
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• Types of leukocytes
– Granulocytes
▪ Granules in their cytoplasm can be stained
▪ Possess lobed nuclei
▪ Include neutrophils, eosinophils, and
basophils

– Agranulocytes
▪ Lack visible cytoplasmic granules
▪ Nuclei are spherical, oval, or kidney-shaped
▪ Include lymphocytes and monocytes

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• List of the WBCs, • Easy way to
from most to least remember this list
abundant:
– Never
– Let
– Neutrophils – Monkeys
– Lymphocytes – Eat
– Monocytes – Bananas
– Eosinophils
– Basophils

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Granulocytes
– Neutrophils
▪ Most numerous WBC (40-70% of WBCs)
▪ Normal count: 3,000–7,000 neutrophils/mm3 of
blood
▪ Numbers increase during infection (Bacterial)
▪ Function as phagocytes (microphages) at active
sites of infection
▪ Multilobed nucleus
▪ Cytoplasm stains pink and contains fine granules

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– Eosinophils
▪ Nucleus stains blue-red
▪ Brick-red cytoplasmic granules
▪ Function is to kill parasitic worms; play a role in
allergy attacks
▪ Normal count: 100–400 eosinophils/mm3 of
blood
▪ 1- 4% of WBCs

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– Basophils
▪ Rarest of the WBCs (0-1% of WBCs)
▪ Normal count: 20–50 basophils/mm3 of blood.
▪ Large histamine-containing granules that stain
dark blue to purple
▪ Contain heparin (anticoagulant)

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Agranulocytes

– Lymphocytes
▪ Large, dark purple nucleus
▪ Slightly larger than RBCs
▪ Reside in lymphatic tissues such as lymph
nodes.
▪ Play a role in immune response
▪ Normal count: 1,500–3,000 lymphocytes/mm3
of blood (20–45% of WBCs)

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– Monocytes
▪ Largest of the white blood cells
▪ Distinctive U- or kidney-shaped dark purple
nucleus
▪ Function as macrophages when they
migrate into tissues
▪ Important in fighting chronic infection
▪ Normal count: 100–700 monocytes/mm3
of blood (4-8% of WBCs)

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• Platelets
– Fragments of megakaryocytes (multinucleate
cells)
– Needed for the clotting process
– Normal platelet count is 300,000 platelets/mm3
of blood
Megakaryocyte

Platelet

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Table 10.2 Characteristics of Formed
Elements of the Blood- Self read

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Hematopoiesis (Blood Cell Formation)

• Hematopoiesis: is the process of blood cell


formation that occurs in red bone marrow.
• All blood cells are derived from a common stem
cell (hemocytoblast)
• Hemocytoblasts form two types of descendants:
a) Lymphoid stem cell: produces lymphocytes
b) Myeloid stem cell: produce all other formed
elements

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Figure 10.3 The Development of Blood Cells

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Formation of Red Blood Cells
(Erythropoiesis)

• Since RBCs are anucleate, they are unable to


divide, grow, or synthesize proteins
• RBCs wear out in 100 to 120 days.
• When worn out, aged RBCs are eliminated by
phagocytes in the spleen or liver.
• Lost cells are replaced by division of
hemocytoblasts in the red bone marrow

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• Reticulocytes are young RBCs which enter the
blood to become oxygen-transporting
erythrocytes

• Rate of RBC production is controlled by a hormone


called erythropoietin.

• Kidneys produce most erythropoietin as a


response to reduced oxygen levels in the
blood.

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• Sites of blood cell formation
– The fetal liver and spleen are early sites of
blood cell formation

– Bone marrow takes over hematopoiesis by


the seventh month

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Concept Link 2-self read
Recall the concept of negative feedback control
(see Chapter 1, p. 41). In this case, erythropoietin is
released in response to a low blood oxygen level,
which stimulates the bone marrow to produce more
red blood cells. With their numbers increased, the
red cells carry more oxygen, increasing the blood
oxygen level and reducing the initial stimulus.

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Figure 10.4 Mechanism for Regulating the Rate of RBC Production

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Formation of White Blood Cells and Platelets
• WBC and platelet production is controlled by
hormones:

– Colony stimulating factors (CSFs) and


interleukins (produced by some WBCs such as
macrophages and lymphocytes) prompt bone
marrow to generate leukocytes (WBCs)

– Thrombopoietin (produced by the liver)


stimulates production of platelets
(thrombocytes) from megakaryocytes.
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Hemostasis

• Hemostasis: is the process of stopping the


bleeding that results from a break (injury) in a
blood vessel.

• Hemostasis involves three phases:


1. Vascular spasms
2. Platelet plug formation
3. Coagulation (blood clotting)

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Step 1: Vascular spasms
– Immediate response to blood vessel injury.
– Vasoconstriction causes blood vessel to spasm.
– Spasms narrow the blood vessel, decreasing blood
loss.

Figure 10.5 Events of Hemostasis


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Step 2: 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 10.5 Events of Hemostasis
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Step 3: Coagulation (Clotting)
– Clotting factors (proteins) present in plasma and
released by injured tissue cells interact with calcium
ions to trigger a clotting cascade
– Prothrombin activator converts prothrombin to
thrombin (an enzyme)
– Thrombin convert fibrinogen (soluble plasma protein)
into fibrin (insoluble hairlike protein). Fibrin forms a
meshwork that traps RBCs and platelets forming the
clot.
– Within the hour, serum (plasma minus (without)
clotting protein) is squeezed from the clot as it retracts
to pull edges of the blood vessel together

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Figure 10.5 Events of Hemostasis Figure 10.6 Fibrin Clot

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

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Disorders of Hemostasis
• Undesirable clotting:
– Thrombus
▪ A clot that develops and persists in an
unbroken blood vessel
▪ Can be deadly in areas such as the lungs

– Embolus
▪ A thrombus that breaks away and floats
freely in the bloodstream
▪ Can later clog vessels in critical areas such
as the brain
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Disorders of Hemostasis
• Bleeding disorders:
– Thrombocytopenia
▪ Insufficient number of circulating platelets
▪ Even normal movements can cause bleeding
from small blood vessels that require platelets for
clotting

– Hemophilia
▪ Hereditary bleeding disorder
▪ Normal clotting factors are missing
▪ Minor tissue damage can cause life-threatening
prolonged bleeding
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Blood Groups and Transfusions

• Large losses of blood have serious consequences


– Loss of 15 to 30 percent causes pallor and
weakness
– Loss of over 30 percent causes shock, which
can be fatal

• Blood transfusions are given for substantial blood


loss, to treat severe anemia, or for
thrombocytopenia

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Human Blood Groups: ABO blood group
– The surface of each red blood cell carries a protein
called an antigen (also called agglutinogen). There
are two antigens:
1. Type A
2. Type B
• ABO blood group:
– Presence of antigen A is called type A
– Presence of antigen B is called type B
– Presence of both antigens A and B is called type AB
– Lack of both antigens A and B is called type O

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• Whereas the blood cell carries antigens, the blood plasma
carries antibodies (called agglutinins) against the antigens of
the other blood types.

• Type A blood has anti-B antibodies.

• Type B blood has anti-A antibodies.

• Type AB blood has no antibodies.

• Type O blood has both anti-A and anti-B antibodies.

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– Type AB can receive A, B, AB, and O blood
▪ Type AB is the “universal recipient”

– Type B can receive B and O blood

– Type A can receive A and O blood

– Type O can receive O blood


▪ Type O is the “universal donor”

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Table 10.3 ABO Blood Groups

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• Transfusions are successful as long as the recipient’s
plasma does not contain antibodies against the ABO type
being transfused.

• If such antibodies are present, they will attack the donor’s


RBCs, causing a transfusion reaction.

• The clumping of RBCs blocks blood vessels, cutting off the


flow of oxygen.

• The RBCs also burst (hemolysis) and release their


hemoglobin into the bloodstream. The free hemoglobin could
block tubules in the kidneys, leading to renal failure and
possibly death. Fever, chills, nausea, and vomiting can also
result .

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View animation on “blood types and transfusion reactions”

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Human Blood Groups: RH blood group

– Rh antigen (agglutinogen D) identified in Rhesus


monkeys.

– Rh-positive blood contains the Rh antigen


– Rh-negative blood lacks this specific antigen.

– Anti-Rh antibodies are not automatically formed in


the blood of Rh-negative individuals (unlike the
antibodies of the ABO system)

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• Someone with Rh-negative blood develops anti-Rh antibodies
after being exposed to Rh-positive blood

• This exposure can happen through a transfusion or when an


Rh-negative mother becomes pregnant with an Rh-positive
fetus).

• If someone with Rh-negative blood receives a transfusion of


Rh-positive blood for first time, the person’s body interprets
the Rh antigen as something foreign. To protect itself, it
develops anti-Rh antibodies but it takes time.

• If the same person receives a second transfusion of Rh-


positive blood, the anti-Rh antibodies formed during the first
transfusion will attack the Rh antigen in the donor blood,
causing agglutination.
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Rh-related problem during pregnancy:
–Danger occurs only when the mother is Rh-, the
father is Rh+ and the child inherits the Rh+
factor.

–RhoGAM® shot (injection) can prevent buildup


of anti-Rh+ antibodies in mother’s blood

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Rh Group
1. First pregnancy 2. Delivery: Blood mixes

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3. Antibody formation 4. Subsequent pregnancy

<<View animation of
blood Rh group, Rh
antibodies, and
erythroblastosis
fetalis>>

View animation of blood Rh group, Rh antibodies, and erythroblastosis fetalis


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• 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)
erythroblastosis fetalis

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Blood Typing
• Blood samples are mixed with anti-A and
anti-B serum
• Agglutination or the lack of agglutination leads
to identification of 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
• Videos of PhysioEx Lab Experiments
https://mediaplayer.pearsoncmg.com/assets/wet-lab-blood-typing

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Figure 10.7 Blood Typing of ABO Blood Groups

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