17: 17
Blood
(RBC)
Chapter Blood
1
Overview of Blood Circulation
Oxygen (O ) and nutrients diffuse across capillary
walls and enter tissues
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 bodys 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 7.357.45
Temperature is 38C, slightly higher than normal body
temperature
Blood accounts for approximately 8% of body weight
Average volume of blood is 56 L for males, and 45 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
Hemoglobin Function binds with oxygen and most
Erythrocyte reversibly
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
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
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
Im b
al a
nce
Start
Normal blood oxygen levels
Im b
al a
nce
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
ietary Requirements of Erythropoiesis
D Erythropoiesis requires:
Proteins, lipids, and carbohydrates
Iron, vitamin B , 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
Chapter 17: Blood
25
Fate and Destruction of Erythrocytes
The life span of an erythrocyte is 100120 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 intoCiron (Fe+3) and biliverdin (green pigment)
28
hapter 17: 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
Impaired iron absorption
Pernicious anemia results from:
12
Deficiency of vitamin B
Lack of intrinsic factor needed for absorption of B12
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 Wrights 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 14% 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 bodys 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 bodys 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 48% 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 numbered are (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
Their granules contain serotonin, Ca , 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
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
Figure 17.12
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, PF , 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
catalyze the conversion of prothrombin to
thrombin
Thrombin
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 PGI 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 A
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
Presence of the Rh agglutinogens on RBCs is
Rh Blood Groups
indicated as Rh
Anti-Rh antibodies are not spontaneously formed in
Rh individuals
Chapter 17: Blood
90
Hemolytic Disease of the Newborn
sensitized Rh mother cross the placenta and attack and
Chapter 17: Blood
91
Transfusion Reactions
Transfusion reactions occur when mismatched blood
is infused
Donors cells are attacked by the recipients 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
Chapter 17: Blood
92
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
Chapter 17: Blood
93
Blood Typing
Blood type being tested
RBC agglutinogens
Serum Reaction
Anti-A
Anti-B
AB
A and B
+
+
B
B
+
A
A
+
O
None
Chapter 17: Blood
94
Plasma Volume Expanders
When shock is imminent from low blood volume,
volume must be replaced
Plasma or plasma expanders can be administered
Chapter 17: Blood
95
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
Chapter 17: Blood
96
Diagnostic Blood Tests
Laboratory examination of blood can assess an
individuals 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 ones general health status in relation to
normal values
Chapter 17: Blood
97