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BLOOD
Chapter 10
Blood
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“river of life”
Transports everything through blood vessels
 Nutrients
 Wastes
 Body
heat
Components of blood
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Only fluid tissue having both solid and liquid
components
It is a complex connective tissue with formed
elements (cells) suspended in nonliving matrix
(plasma)
Erythrocytes (red blood cells)
Buffy coat (leukocytes or white blood cells, and
platelets)
45% RBC, <1% “buffy coat”, 55% plasma
Physical characteristics
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Sticky, opaque fluid
Metallic taste
Ranges from scarlet (oxygen-rich) to dull red (oxygen –
poor)
Heavier than water (due to RBCs) and more viscous
Slightly alkaline, pH 7.35-7.45
Temperature (100.4 F) slightly higher than normal body
temp. (98.6 F)
8% of body weight; in adult males is 5-6 liters (6
quarts)
Plasma
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90% water with >100 different substances
dissolved in it (nutrients, ions (salts), gases, hormones,
proteins, wastes)
Plasma proteins are most abundant solutes
 Most
made by liver
 Variety of functions (maintaining blood pressure to
immunity)
 Are NOT used for metabolic fuel
Erythrocytes
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Red blood cells (RBCs)
Primarily carry oxygen to all cells
Anucleate (Iack a nucleus when mature)
Have few organelles; contain mostly hemoglobin
(iron-containing protein
Use anaerobic methods to make ATP; so RBCs do
NOT consume the oxygen they carry
RBCs
Erythrocytes
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Biconcave disks; flattened with depressed centers
Have large surface area
Outnumber WBCs by 1000 to 1 (5 million cells /
mm3 of blood)
Contribute to blood viscosity
The more hemoglobin contained in RBCs, the more
oxygen can be carried
Normal blood has 12-18 g hemoglobin per 100 mL
blood (men 13-18 g; women 12-16 g)
Homeostatic imbalance

Anemia – decrease in oxygen carrying capacity,
can be caused by (see sickle cell anemia)
 Lower-than-normal
number of RBCs
 Abnormal or deficient hemoglobin content
 See table 10.1 on p. 311
Homeostatic imbalance

Polycythemia – an excessive or abnormal increase
in number of RBCs; can result from
 Bone
marrow cancer
 Response to living at high altitudes
 Causes an increase in blood viscosity and impairs
circulation
Leukocytes
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White blood cells (WBCs)
Less numerous but crucial to defense against disease
Only complete cells in blood (having a nucleus and
organelles)
4000-11000 per mm3
Have the ability to move in / out of blood vessels
(diapedesis)
Leukocytes
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Locate areas of damage or infection by chemical
signals (positive chemotaxis)
Then they “rally” and destroy the foreign substances
WBCs mobilized for action will increase in numbers
(leukocytosis)
Leukopenia is lower than normal WBCs often
caused by drugs or anticancer agents
Homeostatic imbalance

Leukemia-excessive production of abnormal WBCs
 Bone
marrow becomes cancerous
 New WBCs are immature and incapable of defending
the body
 Patient is more susceptible to secondary infection
Leukocytes
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Classified in two categories based on visible
granules
Granulocytes – granules in cytoplasm
 Have
lobed nuclei
 3 forms
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Agranulocytes
 No
visible granules
 Normal nuclei (not lobed)
Granulocytes
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Neutrophils
Multilobed nucleus and fine granules
 Cytoplasm stains pink
 Phagocytes to get rid of infection
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Eosinophils
Blue-red nucleus
 Large red granules
 Numbers increase with allergies or infections of worms
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Basophils
Histamine-containing granules
 Stain dark blue
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Agranulocytes
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Lymphocytes
 Large
dark purple nucleus (most of cell’s volume)
 Contained in lymph tissue, part of immune response
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Monocytes
 Largest
 More
cytoplasm and indented nucleus
 Convert to macrophages when entering tissue
 Fight chronic infections
Platelets
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Not cells
Fragments of multinucleate cells (megakaryocytes)
that rupture releasing the “pieces”
Required for clotting
Hematopoiesis
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Blood cell formation
Occurs in red marrow (myeloid tissue)
In adults: flat bones of skull and pelvis, ribs,
sternum, proximal epiphyses of humerus and femur
After formation, blood cells are sent into blood
Hematopoiesis
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All formed elements (solids) come from one type of
stem cell, hemocytoblast
 Forms
two types of cells
 Lymphoid
stem cell – produces lymphocytes
 Myeloid stem cell – forms all other formed elements
Hematopoiesis
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RBCs are anucleate and cannot synthesize proteins,
grow, or divide
Become rigid at 100-120 days and begin to fragment
Remains are eliminated by spleen and liver
Lost cells are repeatedly replaced by division of
hemocytoblasts
RBCs divide repeatedly then begin to make hemoglobin
 When enough hemoglobin is produced, organelles and
nucleus are ejected and the RBC collapses inward producing
the reticulocyte (still has some ER)
 After 2 days, ER is ejected and they become functional
erythrocytes
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Hematopoiesis
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RBC production takes 3-5 days
Controlled by hormone erythropoietin, produced
mainly by kidneys
Normally, RBCs are produced at constant rate
When blood oxygen levels drop, more
erythropoietin is produced to trigger higher
production of erythrocytes
Hematopoiesis
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Leukocyte and platelet formation controlled by
hormones: colony stimulating factors (CSFs) and
interleukins
These hormones released due to chemical signals,
such as inflammatory chemicals, bacteria, toxins, etc.
Hormones also enhance the immune response
Platelet production is enhanced by thrombopoietin
Hemostasis
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Stopping blood flow
Breakage of a vessel results in reactions to start
hemostasis
Fast and localized process involving components in
blood plasma
Also involves platelets
3 major phases
Platelet plug formation
 Vascular spasms
 Coagulation (clotting)
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Hemostasis
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Platelet plug formation
 Platelets
will stick to a broken area on a vessel
 Anchored platelets release signals to attract more
platelets
 Stack of platelets is a white thrombus
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Vascular spasms
 Anchored
platelets release serotonin which causes the
vessel to spasm
 Spasms narrow the vessel and decrease blood flow and
blood loss
Hemostasis
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Coagulation
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Injured tissue releases thromboplastin (during platelet plug and
spasms)
PF3 (phospholipid) coats the platelets and interacts with
thromboplastin, blood proteins, Ca ions to cause the clotting
cascade
Prothrombin activator converts prothrombin to thromibin (enzyme)
Thrombin joins soluble fibrinogen proteins into long molecules of
insoluble fibrin which traps RBCs to begin the clot
Within an hour, clot retracts, squeezing serum from the mass and
pulling the edges of the vessel together
Clotting normally takes 3-6 minutes, clot triggering factors are
quickly inactivated to prevent widespread clotting
Homeostatic imbalance
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Undesirable clotting
Production of thrombus (clot) in an unbroken vessel
 Can cause fatal heart attacks or stroke
 Caused by poor circulation, burns, physical blows, or fat
accumulation in the vessel
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Bleeding disorders
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Thrombocytopenia (platelet deficiency)
Caused by suppression of myeloid tissue
 Bone marrow cancer, radiation, some drugs
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Hemophilia (lack of clotting factors)
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Genetic disorder (sex-linked recessive)
Human blood groups: transfusions
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Plasma membranes of RBCs have proteins (antigens)
to identify them
An antigen is a substance that a body can
recognize as foreign, which stimulates the immune
system
If the wrong blood type (with different antigens) is
transfused into a patient, the patient’s immune
system will attack the transfused RBCs causing
agglutination (clumping) which will clog small
vessels.
Human blood groups: transfusions
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Transfusion reactions (other than agglutination)
 Kidney
failure
 Fever
 Chills
 Nausea
and vomiting
 Agglutination is the only reaction that is potentially
fatal.
ABO blood groups
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Based (classified) by the 2 antigens that can be
found on the RBCs
Absence of both antigens = type O blood
Presence of both antigens = type AB blood
Presence of only A antigens = type A blood
Presence of only B antigens = type B blood
ABO blood groups
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Antibodies are formed in infancy against the ABO
antigens NOT present on your RBCs
 Type
O people form antibodies against both A and B
antigens
 Type AB people form no ABO antibodies
 Type A people form B antibodies
 Type B people form A antibodies
Rh blood groups
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Named for one of eight Rh antigens (agglutination
D) identified in Rhesus monkeys
Most Americans are Rh+ so RBCs carry Rh antigen
Anti-Rh antibodies are not automatically formed in
infancy (like the ABO groups)
The first “wrong” transfusion will trigger the
production of the anti-Rh antibodies
Subsequent “wrong” transfusions will lead to
agglutination
Rh Blood groups and pregnancy
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Pregnant Rh- women that carry an Rh+ baby
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First pregnancy results in delivery of a healthy baby
Mother becomes sensitized to the Rh+ antigens (and produces
anti-Rh+ antibodies) and must be treated with RhoGAM right
after birth
RhoGAM is an immune serum that prevents the sensitization and
the immune response
If not treated, and she becomes pregnant with another Rh+ baby,
antibodies will cross the placenta and attack the baby’s RBCs
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Hemolytic disease of the newborn
Baby is anemic and hypoxic
Brain damage and death may occur unless the fetus receives
transfusions before birth
Blood typing
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Important to be done before transfusions
Mix blood with different immune serums, anti-A or
anti-B
If agglutination occurs, then that will indicate the
blood type
Developmental aspects
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In embryo, development of the circulatory system occurs
very early (1st trimester)
Blood cell formation starts in the liver and spleen, but
by 7th month has moved primarily to the red marrow
Embryonic blood cells are circulating in blood vessels by
day 28
HbF has a greater ability to pick up oxygen for the
fetus
After birth, fetal blood cells are replaced by RBCs
containing “normal” hemoglobin (HbA)