17
Blood
(RBC)
Chapter 17: Blood
1
Overview of Blood Circulation
 Blood leaves the heart via arteries that branch
repeatedly until they become capillaries
 Oxygen (O2) and nutrients diffuse across capillary
walls and enter tissues
 Carbon dioxide (CO2) and wastes move from tissues
into the blood
Chapter 17: Blood
2
Overview of Blood Circulation
 Oxygen-deficient blood leaves the capillaries and
flows in veins to the heart
 This blood flows to the lungs where it releases CO2
and picks up O2
 The oxygen-rich blood returns to the heart
Chapter 17: Blood
3
Composition of Blood
 Blood is the body’s only fluid tissue
 It is composed of liquid plasma and formed
elements
 Formed elements include:
 Erythrocytes, or red blood cells (RBCs)
 Leukocytes, or white blood cells (WBCs)
 Platelets
 Hematocrit – the percentage of RBCs out of the total
blood volume
Chapter 17: Blood
4
Components of Whole Blood
Plasma
(55% of whole blood)
Buffy coat:
leukocyctes and
platelets
(<1% of whole blood)
1 Withdraw blood
Formed
elements
Erythrocytes
(45% of whole blood)
2 Centrifuge
and place in tube
Chapter 17: Blood
Figure
17.1
5
Physical Characteristics and Volume
 Blood is a sticky, opaque fluid with a metallic taste
 Color varies from scarlet (oxygen-rich) to dark red (oxygenpoor)
 The pH of blood is 7.35–7.45
 Temperature is 38C, slightly higher than “normal” body
temperature
 Blood accounts for approximately 8% of body weight
 Average volume of blood is 5–6 L for males, and 4–5 L for
females
Chapter 17: Blood
6
Functions of Blood
 Blood performs a number of functions dealing with:
 Substance distribution
 Regulation of blood levels of particular substances
 Body protection
Chapter 17: Blood
7
Distribution
 Blood transports:
 Oxygen from the lungs and nutrients from the
digestive tract
 Metabolic wastes from cells to the lungs and
kidneys for elimination
 Hormones from endocrine glands to target organs
Chapter 17: Blood
8
Regulation
 Blood maintains:
 Appropriate body temperature by absorbing and
distributing heat
 Normal pH in body tissues using buffer systems
 Adequate fluid volume in the circulatory system
Chapter 17: Blood
9
Protection
 Blood prevents blood loss by:
 Activating plasma proteins and platelets
 Initiating clot formation when a vessel is broken
 Blood prevents infection by:
 Synthesizing and utilizing antibodies
 Activating complement proteins
 Activating WBCs to defend the body against
foreign invaders
Chapter 17: Blood
10
Blood Plasma
 Blood plasma contains over 100 solutes, including:
 Proteins – albumin, globulins, clotting proteins, and
others
 Nonprotein nitrogenous substances – lactic acid,
urea, creatinine
 Organic nutrients – glucose, carbohydrates, amino
acids
 Electrolytes – sodium, potassium, calcium,
chloride, bicarbonate
 Respiratory gases – oxygen and carbon dioxide
Chapter 17: Blood
11
Formed Elements
 Erythrocytes, leukocytes, and platelets make up the
formed elements
 Only WBCs are complete cells
 RBCs have no nuclei or organelles
 platelets are just cell fragments
 Most formed elements survive in the bloodstream
for only a few days
 Most blood cells do not divide but are renewed by
cells in bone marrow
Chapter 17: Blood
12
Erythrocytes (RBCs)
 Biconcave discs, anucleate, essentially no organelles
 Filled with hemoglobin (Hb), a protein that
functions in gas transport
 Contain the plasma membrane protein spectrin and
other proteins that:
 Give erythrocytes their flexibility
 Allow them to change shape as necessary
Chapter 17: Blood
13
Erythrocytes (RBCs)
Chapter 17: Blood
Figure
17.3
14
Erythrocytes (RBCs)
 Erythrocytes are an example of the complementarity
of structure and function
 Structural characteristics contribute to its gas
transport function
 Biconcave shape that has a huge surface area
relative to volume
 Discounting water content, erythrocytes are more
than 97% hemoglobin
 ATP is generated anaerobically, so the erythrocytes
do not consume the oxygen they transport
Chapter 17: Blood
15
Erythrocyte Function
 Erythrocytes are dedicated to respiratory gas
transport
 Hemoglobin reversibly binds with oxygen and most
oxygen in the blood is bound to hemoglobin
 Hemoglobin is composed of the protein globin,
made up of two alpha and two beta chains, each
bound to a heme group
 Each heme group bears an atom of iron, which can
bind to one oxygen molecule
 Each hemoglobin molecule can transport four
molecules of oxygen
Chapter 17: Blood
16
Structure of Hemoglobin
Chapter 17: Blood
Figure
17.4
17
Hemoglobin
 Oxyhemoglobin – hemoglobin bound to oxygen
 Oxygen loading takes place in the lungs
 Deoxyhemoglobin – hemoglobin after oxygen
diffuses into tissues (reduced Hb)
 Carbaminohemoglobin – hemoglobin bound to
carbon dioxide
 Carbon dioxide loading takes place in the tissues
PLAY
InterActive Physiology®:
Respiratory System: Gas Transport
Chapter 17: Blood
18
Production of Erythrocytes
 Hematopoiesis – blood cell formation
 Hematopoiesis occurs in the red bone marrow of
the:
 Axial skeleton and girdles
 Epiphyses of the humerus and femur
 Hemocytoblasts give rise to all formed elements
Chapter 17: Blood
19
Production of Erythrocytes: Erythropoiesis
 A hemocytoblast is transformed into a committed cell called
the proerythroblast
 Proerythroblasts develop into early erythroblasts
 The developmental pathway consists of three phases
 Phase 1 – ribosome synthesis in early erythroblasts
 Phase 2 – hemoglobin accumulation in late erythroblasts
and normoblasts
 Phase 3 – ejection of the nucleus from normoblasts and
formation of reticulocytes
 Reticulocytes then become mature erythrocytes
Chapter 17: Blood
20
Production of Erythrocytes: Erythropoiesis
Chapter 17: Blood
Figure
17.5
21
Regulation and Requirements for
Erythropoiesis
 Circulating erythrocytes – the number remains
constant and reflects a balance between RBC
production and destruction
 Too few red blood cells leads to tissue hypoxia
 Too many red blood cells causes undesirable blood
viscosity
 Erythropoiesis is hormonally controlled and depends
on adequate supplies of iron, amino acids, and B
vitamins
Chapter 17: Blood
22
Hormonal Control of Erythropoiesis
 Erythropoietin (EPO) release by the kidneys is
triggered by:
 Hypoxia due to decreased RBCs
 Decreased oxygen availability
 Increased tissue demand for oxygen
 Enhanced erythropoiesis increases the:
 RBC count in circulating blood
 Oxygen carrying ability of the blood
Chapter 17: Blood
23
Erythropoietin Mechanism
Start
Normal blood oxygen levels
Increases
O2-carrying
ability of blood
Stimulus: Hypoxia due to
decreased RBC count,
decreased availability of O2
to blood, or increased
tissue demands for O2
Reduces O2
levels in blood
Enhanced
erythropoiesis
increases RBC
count
Erythropoietin
stimulates red
bone marrow
Chapter 17: Blood
Kidney (and liver to a
smaller extent) releases
erythropoietin
24
Figure
17.6
Dietary Requirements of Erythropoiesis
 Erythropoiesis requires:
 Proteins, lipids, and carbohydrates
 Iron, vitamin B12, and folic acid
 The body stores iron in Hb (65%), the liver, spleen,
and bone marrow
 Intracellular iron is stored in protein-iron complexes
such as ferritin and hemosiderin
 Circulating iron is loosely bound to the transport
protein transferrin
Chapter 17: Blood
25
Fate and Destruction of Erythrocytes
 The life span of an erythrocyte is 100–120 days
 Old erythrocytes become rigid and fragile, and their
hemoglobin begins to degenerate
 Dying erythrocytes are engulfed by macrophages
 Heme and globin are separated and the iron is
salvaged for reuse
Chapter 17: Blood
26
Fate and Destruction of Erythrocytes
 Heme is degraded to a yellow pigment called
bilirubin
 The liver secretes bilirubin into the intestines as bile
 The intestines metabolize it into urobilinogen
 This degraded pigment leaves the body in feces, in
a pigment called stercobilin
 Globin is metabolized into amino acids and is
released into the circulation
 Hb released into the blood is captured by
haptoglobin and phgocytized
Chapter 17: Blood
27
Recycling of Hemoglobin
In macrophages of liver or spleen
 globin portion broken down into amino acids & recycled
 heme portion split intoChapter
iron17:(Fe+3)
and biliverdin (green pigment)
28
Blood
Life Cycle of Red Blood Cells
Chapter 17: Blood
Figure
17.7
29
Chapter 17: Blood
Figure
17.7
30
Erythrocyte Disorders
 Anemia – blood has abnormally low oxygencarrying capacity
 It is a symptom rather than a disease itself
 Blood oxygen levels cannot support normal
metabolism
 Signs/symptoms include fatigue, paleness,
shortness of breath, and chills
Chapter 17: Blood
31
Anemia: Insufficient Erythrocytes
 Hemorrhagic anemia – result of acute or chronic
loss of blood
 Hemolytic anemia – prematurely ruptured
erythrocytes
 Aplastic anemia – destruction or inhibition of red
bone marrow
Chapter 17: Blood
32
Anemia: Decreased Hemoglobin Content
 Iron-deficiency anemia results from:
 A secondary result of hemorrhagic anemia
 Inadequate intake of iron-containing foods
 Impaired iron absorption
 Pernicious anemia results from:
 Deficiency of vitamin B12
 Lack of intrinsic factor needed for absorption of B12
 Treatment is intramuscular injection of B12;
application of Nascobal
Chapter 17: Blood
33
Anemia: Abnormal Hemoglobin
 Thalassemias – absent or faulty globin chain in
hemoglobin
 Erythrocytes are thin, delicate, and deficient in
hemoglobin
Chapter 17: Blood
34
Severe, chronic anemias (such as thalassemias and sickle cell
anemia) can increase the bone marrow response to form
RBC's. This drive for erythropoiesis may increase the mass
of marrow and lead to increase in marrow in places, such as
the skull seen here, that is not normally found. Such an
increase in marrow in skull may lead to "frontal bossing" or
forehead prominence because of the skull shape change.
Chapter 17: Blood
35
Anemia: Abnormal Hemoglobin
 Sickle-cell anemia – results from a defective gene coding
for an abnormal hemoglobin called hemoglobin S (HbS)
 HbS has a single amino acid substitution in the beta chain
 This defect causes RBCs to become sickle-shaped in low
oxygen situations
Chapter 17: Blood
36
Anemia: Abnormal Hemoglobin
Chapter 17: Blood
37
Polycythemia
 Polycythemia – excess RBCs that increase blood
viscosity
 Three main polycythemias are:
 Polycythemia vera
 Secondary polycythemia
 Blood doping
Chapter 17: Blood
38
Blood
(WBC and Homeostasis)
Chapter 17: Blood
17
39
Leukocytes (WBCs)
 Leukocytes, the only blood components that are
complete cells:
 Are less numerous than RBCs
 Make up 1% of the total blood volume
 Can leave capillaries via diapedesis
 Move through tissue spaces
 Leukocytosis – WBC count over 11,000 per cubic
millimeter
 Normal response to bacterial or viral invasion
Chapter 17: Blood
40
Granulocytes
 Granulocytes – neutrophils, eosinophils, and
basophils
 Contain cytoplasmic granules that stain specifically
(acidic, basic, or both) with Wright’s stain
 Are larger and usually shorter-lived than RBCs
 Have lobed nuclei
 Are all phagocytic cells
Chapter 17: Blood
41
Basophils
 Account for 0.5% of WBCs and:
 Have U- or S-shaped nuclei with two or three
conspicuous constrictions
 Are functionally similar to mast cells
 Have large, purplish-black (basophilic) granules
that contain histamine
 Histamine – inflammatory chemical that acts as a
vasodilator and attracts other WBCs
(antihistamines counter this effect)
Chapter 17: Blood
42
Eosinophils
 Eosinophils account for 1–4% of WBCs
 Have red-staining, bilobed nuclei connected via a
broad band of nuclear material
 Have red to crimson (acidophilic) large, coarse,
lysosome-like granules
 Lead the body’s counterattack against parasitic
worms
 Lessen the severity of allergies by phagocytizing
immune complexes
Chapter 17: Blood
43
Neutrophils
 Neutrophils have two types of granules that:
 Take up both acidic and basic dyes
 Give the cytoplasm a lilac color
 Contain peroxidases, hydrolytic enzymes, and
defensins (antibiotic-like proteins)
 Neutrophils are our body’s bacteria slayers
Chapter 17: Blood
44
Agranulocytes
 Agranulocytes – lymphocytes and monocytes:
 Lack visible cytoplasmic granules
 Are similar structurally, but are functionally distinct
and unrelated cell types
 Have spherical (lymphocytes) or kidney-shaped
(monocytes) nuclei
Chapter 17: Blood
45
Lymphocytes
 Account for 25% or more of WBCs and:
 Have large, dark-purple, circular nuclei with a thin
rim of blue cytoplasm
 Are found mostly enmeshed in lymphoid tissue
(some circulate in the blood)
 There are two types of lymphocytes: T cells and B
cells
 T cells function in the immune response
 B cells give rise to plasma cells, which produce
antibodies
Chapter 17: Blood
46
Monocytes
 Monocytes account for 4–8% of leukocytes
 They are the largest leukocytes
 They have abundant pale-blue cytoplasms
 They have purple-staining, U- or kidney-shaped
nuclei
 They leave the circulation, enter tissue, and
differentiate into macrophages
Chapter 17: Blood
47
Monocytes
 Macrophages:
 Are highly mobile and actively phagocytic
 Activate lymphocytes to mount an immune
response
Chapter 17: Blood
48
Summary of Formed Elements
Chapter 17: Blood
Table
17.2
49
Summary of Formed Elements
Chapter 17: Blood
Table
17.2
50
Production of Leukocytes
 Leukopoiesis is hormonally stimulated by two
families of cytokines (hematopoietic factors) –
interleukins and colony-stimulating factors (CSFs)
 Interleukins are numbered (e.g., IL-1, IL-2)
 CSFs are named for the WBCs they stimulate (e.g.,
granulocyte-CSF stimulates granulocytes)
 Macrophages and T cells are the most important
sources of cytokines
 Many hematopoietic hormones are used clinically to
stimulate bone marrow
Chapter 17: Blood
51
Formation of Leukocytes
 All leukocytes originate from hemocytoblasts
 Hemocytoblasts differentiate into
 myeloid stem cells
 become myeloblasts or monoblasts
 Myeloblasts develop into eosinophils, neutrophils, and
basophils
 Monoblasts develop into monocytes
 lymphoid stem cells
 Lymphoid stem cells become lymphoblasts
 Lymphoblasts develop into lymphocytes
Chapter 17: Blood
52
Formation of Leukocytes
Chapter 17: Blood
Figure
17.11
53
Leukocytes Disorders: Leukemias
 Leukemia refers to cancerous conditions involving
white blood cells
 Leukemias are named according to the abnormal
white blood cells involved
 Myelocytic leukemia – involves myelocytes
 Lymphocytic leukemia – involves lymphocytes
 Acute leukemia involves blast-type cells and
primarily affects children
 Chronic leukemia is more prevalent in older people
Chapter 17: Blood
54
Leukemia
 Immature white blood cells are found in the
bloodstream in all leukemias
 Bone marrow becomes totally occupied with
cancerous leukocytes
 The white blood cells produced, though numerous,
are not functional
 Death is caused by internal hemorrhage and
overwhelming infections
 Treatments include irradiation, antileukemic drugs,
and bone marrow transplants
Chapter 17: Blood
55
Platelets
 Platelets are fragments of megakaryocytes with a
blue-staining outer region and a purple granular
center
 Their granules contain serotonin, Ca2+, enzymes,
ADP, and platelet-derived growth factor (PDGF)
 Platelets function in the clotting mechanism by
forming a temporary plug that helps seal breaks in
blood vessels
 Platelets (not involved in clotting) are kept inactive
by NO and prostaglandin I2
Chapter 17: Blood
56
Genesis of Platelets
 The stem cell for platelets is the hemocytoblast
 The sequential developmental pathway is
hemocytoblast, megakaryoblast, promegakaryocyte,
megakaryocyte, and platelets
Chapter 17: Blood
57 17.12
Figure
Hematopoiesis
Chapter 17: Blood
58
Hemostasis
 A series of reactions designed for stoppage of
bleeding
 During hemostasis, three phases occur in rapid
sequence
 Vascular spasms
 Platelet plug formation
 Coagulation (blood clotting)
Chapter 17: Blood
59
Vascular Spasm
Immediate vasoconstriction in response to injury
Chapter 17: Blood
60
Platelet Plug Formation

Platelets do not stick to each other or to the endothelial
lining of blood vessels

Upon damage to blood vessel endothelium (which exposes
collagen) platelets:
1. With the help of von Willebrand factor (VWF) adhere
to collagen

Are stimulated by thromboxane A2
2. Stick to exposed collagen fibers and form a platelet
plug
3. Release serotonin and ADP, which attract still more
platelets

The platelet plug is limited to the immediate area of injury
by PGI2
Chapter 17: Blood
61
Platelet Adhesion
Platelets stick to exposed collagen underlying damaged
endothelial cells in vessel wall
Chapter 17: Blood
62
Platelet Release Reaction
Platelets activated by adhesion.
Extend projections to make contact with each other.
Release thromboxane A2 & ADP activating other platelets.
Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through
the injured vessel.
Chapter 17: Blood
63
Platelet Aggregation
Activated platelets stick together and activate new platelets to form a
mass called a platelet plug.
Plug reinforced by fibrin threads formed during clotting process.
Chapter 17: Blood
64
Coagulation

A set of reactions in which blood is transformed
from a liquid to a gel

Coagulation follows intrinsic and extrinsic
pathways

The final three steps of this series of reactions are:
1. Prothrombin activator is formed
2. Prothrombin is converted into thrombin
3. Thrombin catalyzes the joining of fibrinogen into
a fibrin mesh
Chapter 17: Blood
65
Coagulation Phase 1: Two Pathways to
Prothrombin Activator
 May be initiated by either the intrinsic or extrinsic
pathway
 Triggered by tissue-damaging events
 Involves a series of procoagulants
 Each pathway cascades toward factor X
 Once factor X has been activated, it complexes
with calcium ions, PF3, and factor V to form
prothrombin activator
Chapter 17: Blood
66
Coagulation Phase 2: Pathway to Thrombin
 Prothrombin activator catalyzes the transformation
of prothrombin to the active enzyme thrombin
Chapter 17: Blood
67
Coagulation Phase 3: Common Pathways to
the Fibrin Mesh
 Thrombin catalyzes the polymerization of
fibrinogen into fibrin
 Insoluble fibrin strands form the structural basis of a
clot
 Fibrin causes plasma to become a gel-like trap
 Fibrin in the presence of calcium ions activates
factor XIII that:
 Cross-links fibrin
 Strengthens and stabilizes the clot
Chapter 17: Blood
68
Overview of the Clotting Cascade
Prothrombinase is formed by either:
1. intrinsic pathway
2. extrinsic pathway.
Final common pathway produces fibrin
threads.
Chapter 17: Blood
69
Extrinsic Pathway
Damaged tissues leak tissue factor
(thromboplastin) into bloodstream.
In the presence of Ca+2, clotting factor X
combines with factor V to form
prothrombinase.
Prothrombinase forms in seconds.
Chapter 17: Blood
70
Intrinsic Pathway
Activation occurs.
 endothelium is damaged &
platelets come in contact with
collagen of blood vessel wall
 platelets damaged & release
phospholipids
Substances involved: Ca+2 and clotting
factors XII, X and V.
Requires several minutes for reaction to
occur.
Chapter 17: Blood
71
Final Common Pathway
Prothrombinase and Ca+2
 catalyze the conversion of prothrombin to
thrombin
Thrombin
 in the presence of Ca+2 converts soluble
fibrinogen to insoluble fibrin threads
 activates fibrin stabilizing factor XIII
 positive feedback effects of thrombin
 accelerates formation of
prothrombinase
 activates platelets to release
phospholipids
Chapter 17: Blood
72
Clot Retraction and Repair
 Clot retraction
 stabilization of the clot by squeezing serum from
the fibrin strands
 Repair
 Platelet-derived growth factor (PDGF) stimulates
rebuilding of blood vessel wall
 Fibroblasts form a connective tissue patch
 Stimulated by vascular endothelial growth factor
(VEGF), endothelial cells multiply and restore the
endothelial lining
Chapter 17: Blood
73
Factors Limiting Clot Growth or Formation
 Two homeostatic mechanisms prevent clots from
becoming large
 Swift removal of clotting factors
 Inhibition of activated clotting factors
Chapter 17: Blood
74
Inhibition of Clotting Factors
 Fibrin acts as an anticoagulant by:
 binding thrombin
 preventing its:
 Positive feedback effects of coagulation
 Ability to speed up the production of prothrombin
activator via factor V
 Acceleration of the intrinsic pathway by activating
platelets
 Thrombin not absorbed to fibrin is inactivated by
antithrombin III
 Heparin, another anticoagulant, also inhibits thrombin
activity
Chapter 17: Blood
75
Factors Preventing Undesirable Clotting
 Unnecessary clotting is prevented by the structural
and molecular characteristics of endothelial cells
lining the blood vessels
 Platelet adhesion is prevented by:
 The smooth endothelial lining of blood vessels
 Heparin and PGI2 secreted by endothelial cells
 Vitamin E quinone, a potent anticoagulant
Chapter 17: Blood
76
Hemostasis Disorders:
Thromboembolytic Conditions
 Thrombus – a clot that develops and persists in an
unbroken blood vessel
 Thrombi can block circulation, resulting in tissue
death
 Coronary thrombosis – thrombus in blood vessel of
the heart
Chapter 17: Blood
77
Hemostasis Disorders:
Thromboembolytic Conditions
 Embolus – a thrombus freely floating in the blood
stream
 Pulmonary emboli can impair the ability of the
body to obtain oxygen
 Cerebral emboli can cause strokes
Chapter 17: Blood
78
Prevention of Undesirable Clots
 Substances used to prevent undesirable clots
include:
 Aspirin – an antiprostaglandin that inhibits
thromboxane A2
 Heparin – an anticoagulant used clinically for preand postoperative cardiac care
 Warfarin – used for those prone to atrial fibrillation
Chapter 17: Blood
79
Hemostasis Disorders
 Disseminated Intravascular Coagulation (DIC):
widespread clotting in intact blood vessels
 Residual blood cannot clot
 Blockage of blood flow and severe bleeding follows
 Most common as:
 A complication of pregnancy
 A result of septicemia or incompatible blood
transfusions
Chapter 17: Blood
80
Hemostasis Disorders: Bleeding Disorders
 Thrombocytopenia – condition where the number of
circulating platelets is deficient
 Patients show petechiae (small purple blotches on
the skin) due to spontaneous, widespread
hemorrhage
 Caused by suppression or destruction of bone
marrow (e.g., malignancy, radiation)
 Platelet counts less than 50,000/mm3 is diagnostic
for this condition
 Treated with whole blood transfusions
Chapter 17: Blood
81
Hemostasis Disorders: Bleeding Disorders
 Inability to synthesize procoagulants by the liver
results in severe bleeding disorders
 Causes can range from vitamin K deficiency to
hepatitis and cirrhosis
 Inability to absorb fat can lead to vitamin K
deficiencies as it is a fat-soluble substance and is
absorbed along with fat
 Liver disease can also prevent the liver from
producing bile, which is required for fat and vitamin
K absorption
Chapter 17: Blood
82
Hemostasis Disorders: Bleeding Disorders
 Hemophilias – hereditary bleeding disorders caused
by lack of clotting factors
 Hemophilia A – most common type (83% of all
cases) due to a deficiency of factor VIII
 Hemophilia B – results from a deficiency of factor
IX
 Hemophilia C – mild type, caused by a deficiency
of factor XI
Chapter 17: Blood
83
Hemostasis Disorders: Bleeding Disorders
 Symptoms include prolonged bleeding and painful
and disabled joints
 Treatment is with blood transfusions and the
injection of missing factors
Chapter 17: Blood
84
Blood Transfusions
 Whole blood transfusions are used:
 When blood loss is substantial
 In treating thrombocytopenia
 Packed red cells (cells with plasma removed) are
used to treat anemia
Chapter 17: Blood
85
Human Blood Groups
 RBC membranes have glycoprotein antigens on their
external surfaces
 These antigens are:
 Unique to the individual
 Recognized as foreign if transfused into another individual
 Promoters of agglutination and are referred to as
agglutinogens
 Presence or absence of these antigens is used to classify
blood groups
Chapter 17: Blood
86
Blood Groups
 Humans have 30 varieties of naturally occurring
RBC antigens
 The antigens of the ABO and Rh blood groups cause
vigorous transfusion reactions when they are
improperly transfused
 Other blood groups (M, N, Dufy, Kell, and Lewis)
are mainly used for legalities
Chapter 17: Blood
87
ABO Blood Groups
 The ABO blood groups consists of:
 Two antigens (A and B) on the surface of the RBCs
 Two antibodies in the plasma (anti-A and anti-B)
 An individual with ABO blood may have various
types of antigens and spontaneously preformed
antibodies
 Agglutinogens and their corresponding antibodies
cannot be mixed without serious hemolytic reactions
Chapter 17: Blood
88
ABO Blood Groups
Chapter 17: Blood
Table
17.4
89
Rh Blood Groups
 There are eight different Rh agglutinogens, three of
which (C, D, and E) are common
 Presence of the Rh agglutinogens on RBCs is
indicated as Rh+
 Anti-Rh antibodies are not spontaneously formed in
Rh– individuals
 However, if an Rh– individual receives Rh+ blood,
anti-Rh antibodies form
 A second exposure to Rh+ blood will result in a
typical transfusion reaction
Chapter 17: Blood
90
Hemolytic Disease of the Newborn
 Hemolytic disease of the newborn – Rh+ antibodies of a
sensitized Rh– mother cross the placenta and attack and
destroy the RBCs of an Rh+ baby
 Rh– mother becomes sensitized when Rh+ blood (from a
previous pregnancy of an Rh+ baby or a Rh+ transfusion)
causes her body to synthesis Rh+ antibodies
 The drug RhoGAM can prevent the Rh– mother from
becoming sensitized
 Treatment of hemolytic disease of the newborn involves prebirth transfusions and exchange transfusions after birth
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Transfusion Reactions
 Transfusion reactions occur when mismatched blood
is infused
 Donor’s cells are attacked by the recipient’s plasma
agglutinins causing:
 Diminished oxygen-carrying capacity
 Clumped cells that impede blood flow
 Ruptured RBCs that release free hemoglobin into
the bloodstream
 Circulating hemoglobin precipitates in the kidneys
and causes renal failure
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Blood Typing
 When serum containing anti-A or anti-B agglutinins
is added to blood, agglutination will occur between
the agglutinin and the corresponding agglutinogens
 Positive reactions indicate agglutination
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Blood Typing
Blood type being tested
RBC agglutinogens
Serum Reaction
Anti-A
Anti-B
AB
A and B
+
+
B
B
–
+
A
A
+
–
O
None
–
–
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Plasma Volume Expanders
 When shock is imminent from low blood volume,
volume must be replaced
 Plasma or plasma expanders can be administered
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Plasma Volume Expanders
 Plasma expanders
 Have osmotic properties that directly increase fluid
volume
 Are used when plasma is not available
 Examples: purified human serum, albumin,
plasminate, and dextran
 Isotonic saline solution can also be used to replace
lost blood volume
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Diagnostic Blood Tests
 Laboratory examination of blood can assess an
individual’s state of health
 Microscopic examination:
 Variations in size and shape of RBCs – predictions
of anemias
 Type and number of WBCs – diagnostic of various
diseases
 Chemical analysis can provide a comprehensive
picture of one’s general health status in relation to
normal values
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