BLOOD
Physical Characteristics
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Color depends on oxygen
content
8% of body weight
4 - 5 L in females, 5 - 6 L in
males
pH – slightly alkaline
(7.35 – 7.45)
About 100.4° F
With
O2
Without
O2
What Is It?
What Is It?

55% plasma
is 90% water – solvent, heat
absorber
 Plasma proteins
 Plasma
 Albumin
– osmotic balance, pH
buffering
 Fibrinogen – blood clotting
 Globulins – defense (antibodies), lipid
transport
(electrolytes) – osmotic
balance, pH buffering
 Salts
What Is It?
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45% formed elements (living cells)
 Buffy
coat = less than 1%
 Leukocytes
(white blood cells)
 Platelets
 Erythrocytes
 More
(red blood cells)
than 99%
 Percentage of total blood volume =
hematocrit
Erythrocytes
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Transport oxygen to cells
Tiny - 4-6 million /mm3 of blood
Produced in bone marrow
Life span is 100-120 days
Biconcave (Why?)
Anucleate
No organelles (How do they get
energy?)
Erythrocytes
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97% of solid material is
hemoglobin
 Anemia
– reduced oxygen levels
 low
# of erythrocytes
 low amounts of hemoglobin
 Sickle-cell
 Mutation
anemia
in hemoglobin gene
 Reduced malaria risk
Normal vs. Iron Deficiency Anemia
Normal vs. Sickle Cell Anemia
Leukocytes
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Defend against disease
Produced in bone marrow
Perform diapedesis
Types of Leukocytes

Granulocytes – contain granules
 Neutrophils
 Most
numerous WBC (~60%)
 Multi-lobed nucleus & pale granules
 Kill bacteria
 Eosinophils
 Bi-lobed
nucleus, reddish granules
 Kill parasitic worms
 Basophils
 Bluish
granules
 Inflammatory response
Types of Leukocytes
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Agranulocytes – lack granules
 Lymphocytes
 About
30% WBC
 One large nucleus
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2 Types: T Cells
& B Cells
Monocytes
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Largest WBC with pale U-shaped nucleus
Become macrophages – “cell eaters”
Normal vs. Leukemia
Platelets
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Small cell fragments
Responsible for blood clotting
Sketch & Label
Hemostasis – 3 Phases
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Phase One: Platelet plug formation
Damage to a
blood vessel
Exposes
collagen fibers
Chemicals
attract more
platelets
Platelets stick
to collagen and
release
chemicals
Hemostasis – 3 Phases
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Phase Two: Vascular spasms
 Platelets
release serotonin, causing the blood
vessel to spasm and narrow.
How is this
helpful?
Hemostasis – 3 Phases
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Phase Three: Coagulation
A “clotting cascade” is triggered:
 Damaged tissues release TF (tissue factor)
 TF combines with vitamins, ions and clotting
factors in the plasma and platelet plug to form
prothrombin activator
 Prothrombin activator converts prothrombin in
plasma to thrombin
 Thrombin joins together soluble fibrinogen
proteins into long insoluble molecules of fibrin
Tissue
Damage
(TF)
Factors in blood
(clotting proteins,
Vitamin K, calcium)
Platelet Plug
(PF3)
Prothrombin
Activator
Prothrombin
Thrombin
Fibrinogen
(soluble)
Fibrin
(insoluble)
Clotting Cascade (continued)
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Fibrin traps red blood cells & contracts,
squeezing out plasma & sealing blood vessels
Question to consider…
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When you have an open wound, why should
you apply gauze and pressure?
Disorders of Hemostasis
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Hemophilia
Disorders of Hemostasis
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Thrombus
Embolus
Blood Typing - Antigens
Blood Typing - Antibodies
To clarify…
Blood Typing - Agglutination
Blood Typing
Hematopoiesis
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Blood cell formation
In red bone marrow
 Axial
skeleton
 Pelvic and pectoral girdles
 Humerus & femur
Hemocytoblasts
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Stem cells that make all formed elements
Erythropoiesis
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Red blood cell production
3 phases:
1.
2.
3.
Ribosome synthesis – used to produce
hemoglobin
Hemoglobin accumulates
Nucleus and organelles are ejected
Erythropoietin
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Hormone that stimulates erythropoiesis;
increases RBC production
Produced by the kidneys
Release controlled by negative feedback
The balance
between RBC
production and
destruction is
very important!!
Why?
Events causing release of erythropoietin…
Decreased RBC count
2. Decreased availability of oxygen
3. Increased tissue demands for oxygen
What is the variable that is being monitored?
1.
The Spleen
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Graveyard for RBC’s
Dying erythrocytes are
engulfed and destroyed by
macrophages
Hemoglobin gets reused
Why do erythrocytes
die of old age?
Questions for thought…
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How would
spending time on
the upper slopes
of K2 (at right)
affect your body’s
erythropoietin
levels?
How would it
affect your blood
viscosity?
Questions for thought…
What changes
would you expect to
see in an athlete
who trains at high
altitudes?
Do you think these
are a benefit or
detriment to sealevel performance?
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Questions for thought…
Blood-Doping –
illegally boosting the
number of RBCs in
circulation in order to
enhance athletic
performance
Do you think this should
be illegal?
How does it differ from
high altitude training?
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