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Artery
White blood cells
Platelets
Red blood cells
• Deliver O2
• Remove metabolic wastes
• Maintain temperature, pH, and fluid volume
• Protection from blood loss- platelets
• Prevent infection- antibodies and WBC
• Transport hormones
Plasma-55%
Buffy coat-<1%
Formed
elements-45%
90% Water
8% Solutes:
• Proteins
Albumin (60 %)
Alpha and Beta Globulins
Gamma Globulins
fibrinogens
• Gas
• Electrolytes
• Organic Nutrients
Carbohydrates
Amino Acids
Lipids
Vitamins
• Hormones
• Metabolic waste
CO2
Urea
• Leukocytes
• Platelets
• Erythrocytes (red blood cells)
• Leukocytes (white blood cells)
• Platelets (thrombocytes)
Erythrocytes
Erythrocyte7.5m in dia
 Anucleate- so can't reproduce; however, repro
in red bone marrow
 Hematopoiesis- production of RBC
 Function- transport respiratory gases
 Hemoglobin- quaternary structure, 2  chains
and 2  chains
 Lack mitochondria. Why?
 1 RBC contains 280 million hemoglobin
molecules
 Men- 5 million cells/mm3
 Women- 4.5 million cells/mm3
 Life span 100-120 days and then destroyed in
spleen (RBC graveyard)
Hemoglobin
Hematopoiesis
• Hematopoiesis (hemopoiesis):
blood cell formation
–Occurs in red bone marrow of
axial skeleton, girdles and
proximal epiphyses of humerus
and femur
Hematopoiesis
• Hemocytoblasts (hematopoietic stem
cells)
– Give rise to all formed elements
– Hormones and growth factors push the cell
toward a specific pathway of blood cell
development
• New blood cells enter blood sinusoids
Erythropoiesis
• Erythropoiesis: red blood cell
production
– A hemocytoblast is transformed into a
proerythroblast
– Proerythroblasts develop into early
erythroblasts
Erythropoiesis
– Phases in development
1. Ribosome synthesis
2. Hemoglobin accumulation
3. Ejection of the nucleus and
formation of reticulocytes
– Reticulocytes then become
mature erythrocytes
Stem cell
Hemocytoblast
Committed
cell
Developmental pathway
Proerythroblast
Early
Late
erythroblast erythroblast
Phase 1
Ribosome
synthesis
Phase 2
Hemoglobin
accumulation
Phase 3
Ejection of
nucleus
Normoblast
Reticulo- Erythrocyte
cyte
Figure 17.5
Regulation of Erythropoiesis
• Too few RBCs leads to tissue hypoxia
• Too many RBCs increases blood
viscosity
• Balance between RBC production and
destruction depends on
– Hormonal controls
– Adequate supplies of iron, amino acids,
and B vitamins
Hormonal Control of
Erythropoiesis
• Erythropoietin (EPO)
–Direct stimulus for erythropoiesis
–Released by the kidneys in
response to hypoxia
Hormonal Control of
Erythropoiesis
• Causes of hypoxia
– Hemorrhage or increased RBC destruction
reduces RBC numbers
– Insufficient hemoglobin (e.g., iron
deficiency)
– Reduced availability of O2 (e.g., high
altitudes)
Hormonal Control of
Erythropoiesis
• Effects of EPO
– More rapid maturation of committed bone
marrow cells
– Increased circulating reticulocyte count in
1–2 days
• Testosterone also enhances EPO
production, resulting in higher RBC
counts in males
Formation & Destruction of RBCs
Blood Cell Production
RBC Diseases
Anemia- when blood has low O2 carrying
capacity; insufficient RBC or iron deficiency.
Factors that can cause anemia- low iron, B12
deficiency
RBC Diseases
Sickle-cell anemia-
•HbS results from a change in just one of the 287
amino acids in the  chain in the globin molecule.
•Found in 1 out of 400 African Americans.
•Homozygous for sickle-cell is deadly, but in malaria
infested countries, the heterozygous condition is
beneficial.
RBC Diseases
Polycythemia- excess of erythrocytes, 
viscosity of blood;
8-11 million cells/mm3
Usually caused by cancer; however, naturally
occurs at high elevations
Blood doping- in athletesremove blood 2
days before event and then replace it- banned
by Olympics.
4,000-11,000 cells/mm 3
Never let monkeys eat bananas
Granulocytes
Neutrophils- 40-70%
Eosinophils- 1-4%
Basophils- <1%
Agranulocytes
Monocytes- 4-8%
Lymphocytes- 20-45%
Basophil
Eosinophil
Lymphocyte
platelet
Neutrophil
Monocyte
ID WBC’s
White Blood Cells
• Protect body against microorganisms and
remove dead cells and debris
• Movements
Ameboid
Diapedesis
Chemotaxis
Passive Immunity
Active Immunity
Antigen – Antibody
What do T- and B-cells do?
Above show T cells
http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbody/whatdo
esyourimmunesystemdo/howdoesyourimmunesystemwork/whatdot-andbcellsdo.aspx
T- and B-cells are highly specialized
defender cells - different groups of
cells are tailored to different germs.
When your body is infected with a
particular germ, only the T- and Bcells that recognize it will respond.
These selected cells then quickly
multiply, creating an army of
identical cells to fight the infection.
Special types of T- and B-cells
'remember' the invader, making you
immune to a second attack.
Left shows T cells top and
E-Coli below
T- and B-cells recognize invaders by
the shape of molecules - antigens on their surfaces. Your immune
system can produce a T- and B-cell
to fit every possible shape.
However, any T- or B-cell that
recognized molecules found on
your cells were destroyed while you
were growing in the womb, to
prevent them from attacking your
own body. But you were left with
millions of others, one for every
foreign antigen you might ever
encounter.
Left shows T cell (orange) attacking a
cancer cell
http://www.sciencemuseum.org.uk/whoami/findoutmore/your
body/whatdoesyourimmunesystemdo/howdoesyourimmunes
ystemwork/whatdot-andb-cellsdo.aspx
Having recognized the invader,
different types of T-cell then have
different jobs to do. Some send
chemical instructions (cytokines) to
the rest of the immune system. Your
body can then produce the most
effective weapons against the
invaders, which may be bacteria,
viruses or parasites. Other types of Tcells recognize and kill virus-infected
cells directly. Some help B-cells to
make antibodies, which circulate and
bind to antigens.
Left shows the molecular structure of
an antibody.
http://www.sciencemuseum.org.uk/whoami/findoutmore/yourbody/whatdoesy
ourimmunesystemdo/howdoesyourimmunesystemwork/whatdot-andbcellsdo.aspx
With the help of T-cells, Bcells make special Y-shaped
proteins called antibodies.
Antibodies stick to antigens
on the surface of germs,
stopping them in their tracks,
creating clumps that alert
your body to the presence of
intruders. Your body then
starts to make toxic
substances to fight them.
Patrolling defender cells
called phagocytes engulf and
destroy antibody-covered
intruders
Leukocyte Squeezing Through Capillary Wall
WBCs Moving out of the blood stream
•
Leukopenia
•
•
Abnormally low WBC count—drug induced
Leukemias
•
Cancerous conditions involving WBCs
•
Named according to the abnormal WBC
clone involved
• Mononucleosis
•
highly contagious viral disease caused by
Epstein-Barr virus; excessive # of
agranulocytes; fatigue, sore throat, recover
in a few weeks
White Blood Cells
Types
Neutrophils: Most common; phagocytic cells
destroy bacteria (60%)
Eosinophils: Detoxify chemicals; reduce
inflammation (4%)
Basophils: Alergic reactions; Release histamine,
heparin increase inflam. response (1%)
Lymphocytes: Immunity 2 types; b & t Cell types.
IgG-infection, IgM-microbes, IgA-Resp & GI, IgEAlergy, IgD-immune response
Monocytes: Become macrophages
Platelets
• Small fragments of megakaryocytes
• Formation is regulated by
thrombopoietin
• Blue-staining outer region, purple
granules
• Granules contain serotonin, Ca2+,
enzymes, ADP, and platelet-derived
growth factor (PDGF)
Stem cell
Developmental pathway
Hemocytoblast
Promegakaryocyte
Megakaryoblast
Megakaryocyte
Platelets
Figure 17.12
Hemostasis- stoppage of bleeding
Platelets: 250,000-500,000 cells/mm3
Tissue Damage
Platelet Plug
Clotting Factors
Hemostasis:
1. Vessel injury
2. Vascular spasm
3. Platelet plug formation
4. Coagulation
Hemostasis
(+ feedback)
Clotting Factors
thromboplastin
Prothrombin
Thrombin
Fibrinogen
Fibrin
Traps RBC & platelets
Platelets release thromboplastin
Blood
Clot
RBC
Does this look like
spider webs?
Platelet
Fibrin thread
Disorders of Hemostasis
• Thromboembolytic disorders:
undesirable clot formation
• Bleeding disorders: abnormalities that
prevent normal clot formation
Thromboembolytic Conditions
• Thrombus: clot that develops and persists in
an unbroken blood vessel
– May block circulation, leading to tissue death
• Embolus: a thrombus freely floating in the
blood stream
– Pulmonary emboli impair the ability of the body to
obtain oxygen
– Cerebral emboli can cause strokes
Thromboembolic Conditions
• Prevented by
– Aspirin
• Antiprostaglandin that inhibits
thromboxane A2
– Heparin
• Anticoagulant used clinically for pre- and
postoperative cardiac care
– Warfarin
• Used for those prone to atrial fibrillation
Thrombocytosis- too many platelets due to
inflammation, infection or cancer
Thrombocytopenia- too few platelets
• causes spontaneous bleeding
• due to suppression or destruction of bone
marrow (e.g., malignancy, radiation)
– Platelet count <50,000/mm3 is diagnostic
– Treated with transfusion of concentrated
platelets
• Impaired liver function
– Inability to synthesize procoagulants
– Causes include vitamin K deficiency,
hepatitis, and cirrhosis
– Liver disease can also prevent the
liver from producing bile, impairing fat
and vitamin K absorption
• Hemophilias include several similar
hereditary bleeding disorders
• Symptoms include prolonged
bleeding, especially into joint
cavities
• Treated with plasma transfusions
and injection of missing factors
Hemophiliac- a sex-linked recessive trait, primarily
carried by males (x chromosome)
Type A
Type B
Type AB
Type O
Blood type is based on the presence of 2 major antigens in
RBC membranes-- A and B
Blood type
Antigen
Antibody
A
A
anti-B
B
B
anti-A
A&B
AB
no anti body
Neither A or B
O
anti-A and anti-B
Antigen- protein on the surface of a RBC membrane
Antibody- proteins made by lymphocytes in plasma which are
made in response to the presence of antigens.
They attack foreign antigens, which result in clumping
(agglutination)
Type A
b
b
b
b
b
b
b
Type B
a
a
a
a
a
a
a
Type O
a
b
a
a
a
b
b
a
a
b
Type AB
Rh Factor and Pregnancy
RH+ indicates protein
RH- indicates no protein
Rh Factor
and
Pregnancy
Rh+ mother w/Rh- baby– no problem
Rh- mother w/Rh+ baby– problem
Rh- mother w/Rh- father– no problem
Rh- mother w/Rh- baby-- no problem
RhoGAM used @ 28 weeks
Type AB- universal recipients
Type O- universal donor
Rh factor:
Rh+ 85% dominant in pop
Rh- 15% recessive
Blood Type
Clumping
Antibody
A
antigen A
anti-A serum
antibody anti-b
B
antigen B
anti-B serum
antibody anti-a
AB
antigen A & B
anti A & B serum
O
neither A or B
no clumping w/ either anti A or B anti-a, anti-b
-
Blood being tested
Type AB (contains
agglutinogens A and B;
agglutinates with both
sera)
Anti-A
Serum
Anti-B
RBCs
Type A (contains
agglutinogen A;
agglutinates with anti-A)
Type B (contains
agglutinogen B;
agglutinates with anti-B)
Type O (contains no
agglutinogens; does not
agglutinate with either
serum)
Figure 17.16
Blood Type & Rh
How Many Have It
O
O
A
A
B
B
AB
AB
1 person in 3
1 person in 15
1 person in 3
1 person in 16
1 person in 12
1 person in 67
1 person in 29
1 person in 167
Rh Positive
Rh Negative
Rh Positive
Rh Negative
Rh Positive
Rh Negative
Rh Positive
Rh Negative
Frequency
37.4%
6.6%
35.7%
6.3%
8.5%
1.5%
3.4%
.6%
ABO Blood Types
Phenotype Genotype
O
i i
A
I A I A or I A i
B
I B I B or I B i
A
B
AB
I I
Punnett square
Type A and Type B cross
IA
IA
IB
i
IA IB
IAi
IA IB
IA i