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Blood
Introduction
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Blood Cells
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form mostly in red bone marrow
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red blood cells (erythrocytes)
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white blood cells (Leukocytes)
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platelets (cell fragments)
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Classified as a connective tissue
Functions of Blood
Distribution of
1.
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O2 and nutrients to body cells
Metabolic wastes to the lungs and kidneys for
elimination
Hormones from endocrine organs to target
organs
Functions of Blood
Regulation of
2.
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Body temperature by absorbing and distributing
heat
Normal pH using buffers
Adequate fluid volume in the circulatory system
Functions of Blood
Protection against
3.
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Blood loss
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Plasma proteins and platelets initiate clot formation
Infection
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Antibodies
Complement proteins
WBCs defend against foreign invaders
Volume
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varies with
 body size
 changes in fluid concentration
 changes in electrolyte concentration
 amount of adipose tissue
about 8% of body weight
about 5 liters 5-6 (M) 4-5 L (F)
pH 7.35-7.45
RBC’s
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erythrocytes
biconcave = surface
area
one-third hemoglobin:
oxyhemoglobin-red
deoxyhemoglobin-blue
lack nuclei and
mitochondria
Function to carry
oxygen
Outnumber WBC
Cont….
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RBC Count: # of RBC per cubic millimeter of blood
Males- 4,600,000 – 6,200,000 per ul
Females- 4,200,000 – 5,400,000 per ul
Children- 4,500,000 – 5,100,000
So overall who should run the farthest?????
How are they Made: low blood oxygen causes
kidneys and liver to release erythropoietin which
stimulates RBC production in the bone marrow.
Erythrocyte Function
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Hemoglobin structure
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Protein globin: two alpha and two beta chains
Heme pigment bonded to each globin chain
Each RBC carries about 250 million
Iron atom in each heme can bind to one O2
molecule
Each Hb molecule can transport four O2
b Globin chains
Heme
group
a Globin chains
(a) Hemoglobin consists of globin (two
alpha and two beta polypeptide
chains) and four heme groups.
(b) Iron-containing heme pigment.
Figure 17.4
Hemoglobin (Hb)
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O2 loading in the lungs
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O2 unloading in the tissues
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Produces oxyhemoglobin (ruby red)
Produces deoxyhemoglobin or reduced
hemoglobin (dark red)
CO2 loading in the tissues

Produces carbaminohemoglobin (carries
20% of CO2 in the blood)
Cont….
Homeostasis: Normal blood oxygen levels
1 Stimulus:
5
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased
RBC count
• Decreased amount
of hemoglobin
• Decreased
availability of O2
O2- carrying
ability of blood
increases.
2
4
Enhanced
erythropoiesis
increases RBC
count.
3
Kidney (and liver to
a smaller extent)
releases
erythropoietin.
Erythropoietin
stimulates red
bone marrow.
Figure 17.6
Regulation of Erythropoiesis
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Too few RBCs leads to tissue hypoxia
Too many RBCs increases blood
viscosity
Balance between RBC production and
destruction depends on

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Hormonal controls
Adequate supplies of iron, amino acids,
and B vitamins
Life Cycle
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Live about 120
days
Makes 75,000 trips
Old RBC are
destroyed in the
spleen and liver by
macrophages
Hemoglobin is
broken down and
the iron from it
returns to bone
marrow
Anemia
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aplastic anemia: bone marrow damaged, toxic
chemicals, radiation
hemolytic anemia: RBCs destroyed, toxic chemicals
sickle cell anemia: abnormal shape of RBCs, defective
gene
iron deficiency anemia: hemoglobin deficient, lack of
iron
pernicious anemia: excess of immature RBCs, inability
to absorb B12 can cause brain damage
Thalassemia: hemoglobin deficient, RBCs short-lived,
defective gene
(a) Normal erythrocyte has normal
hemoglobin amino acid sequence
in the beta chain.
1
2
3
4
5
6
7
146
(b) Sickled erythrocyte results from
a single amino acid change in the
beta chain of hemoglobin.
1
2
3
4
5
6
7
146
Figure 17.8
(a) Neutrophil;
multilobed
nucleus
(b) Eosinophil;
bilobed nucleus,
red cytoplasmic
granules
(c) Basophil;
bilobed nucleus,
purplish-black
cytoplasmic
granules
Figure 17.10 (a-c)
(d) Small
lymphocyte;
large spherical
nucleus
(e) Monocyte;
kidney-shaped
nucleus
Figure 17.10d, e
Leukocyte Disorders
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Leukopenia
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Leukemias
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Abnormally low WBC count—drug induced
Cancerous conditions involving WBCs
Named according to the abnormal WBC clone
involved
Myelocytic leukemia involves myeloblasts
Lymphocytic leukemia involves lymphocytes
Acute leukemia involves blast-type cells and
primarily affects children
Chronic leukemia is more prevalent in older
people
Leukemia
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Bone marrow totally occupied with
cancerous leukocytes
Immature nonfunctional WBCs in the
bloodstream
Death caused by internal hemorrhage
and overwhelming infections
Treatments include irradiation,
antileukemic drugs, and stem cell
transplants
Diapadesis
Plasma
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90% water and 55% of blood volume
Plasma Proteins: Albumins 60% help maintain
osmotic pressure of blood. Hold water in
capillaries with colloid pressure
Fibrinogen 4% originate in liver, plays key role
in blood coagulation
Alpha and Beta Globulins originate in liver,
transport lipids and fat-soluble vitamins
Gamma Globulins originate in lymphatic
tissues, constitute the antibodies of immunity
Globulins = 36%
Cont…
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Plasma Gases: oxygen, carbon dioxide, nitrogen
Plasma Nutrients: amino acids, simple sugars,
nucleotides, lipids, lipoproteins
Hormones
Plasma Lipoproteins: Chylomicrons high concentration
of triglycerides, transport dietary fats to muscles and
adipose cells
LDLs high concentration of cholesterol, deliver
cholesterol to various cells
VLDLs high concentration of triglycerides, produced in
the liver, transport triglycerides from liver to adipose cells
and converted by enzyme into LDL
Cont….
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HDLs high concentration of proteins, come from
LDLs who have dumped their cholestero,l
Nonprotein nitrogenous substances: urea –
product of protein catabolism; about 50% of
NPN substances
uric acid – product of nucleic acid catabolism
amino acids – product of protein catabolism
creatine – stores phosphates used for energy
creatinine – product of creatine metabolism
BUN – blood urea nitrogen; indicate health of
kidney since kidney excretes the urea
Plasma electrolytes
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sodium
potassium
calcium
magnesium
chloride
bicarbonate
phosphate
sulfate
sodium and potassium most abundant
Stopping Bleeding
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Hemostasis involves three phases
 1. Platelet plug formation
 2. Vascular spasms
 3. Coagulation
1. Collagen fibers are exposed by a break in a blood
vessel
Platelets become “sticky” and cling to fibers
Anchored platelets release chemicals to attract more
platelets
Platelets pile up to form a platelet plug
Cont…
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2. Anchored platelets release serotonin
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Serotonin causes blood vessel muscles to spasm
Spasms narrow the blood vessel, decreasing blood loss
3. Injured tissues release thromboplastin
PF3 (a phospholipid) interacts with thromboplastin, blood
protein clotting factors, and calcium ions to trigger a
clotting cascade
Prothrombin activator converts prothrombin to thrombin
(an enzyme) Thrombin joins fibrinogen proteins into hairlike fibrin
Fibrin forms a meshwork
(the basis for a clot)
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Step 1 Vascular spasm
• Smooth muscle contracts,
causing vasoconstriction.
Collagen
fibers
Step 2 Platelet plug
formation
• Injury to lining of vessel
exposes collagen fibers;
platelets adhere.
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
Platelets
Fibrin
Step 3 Coagulation
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Figure 17.13
Figure 17.15
Blood Clotting
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Blood usually clots within 3 to 6
minutes
The clot remains as endothelium
regenerates
The clot is broken down after tissue
repair
Clot Repair
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Platelet-derived growth factor (PDGF)
stimulates division of smooth muscle
cells and fibroblasts to rebuild blood
vessel wall
Vascular endothelial growth factor
(VEGF) stimulates endothelial cells to
multiply and restore the endothelial
lining
Fibrinolysis
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Begins within two days
Plasminogen in clot is converted to
plasmin by tissue plasminogen
activator (tPA), factor XII and thrombin
Plasmin is a fibrin-digesting enzyme
Undesirable Clotting
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Thrombus
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A clot in an unbroken blood vessel
Can be deadly in areas like the heart
Embolus
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A thrombus that breaks away and floats
freely in the bloodstream
Can later clog vessels in critical areas such
as the brain
Bleeding Disorders
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Thrombocytopenia
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Platelet deficiency
Even normal movements can cause bleeding
from small blood vessels that require
platelets for clotting
Hemophilia
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Hereditary bleeding disorder
Normal clotting factors are missing
Blood Groups and
Transfusions
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Large losses of blood have serious
consequences
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Loss of 15 to 30 percent causes weakness
Loss of over 30 percent causes shock, which can
be fatal
Transfusions are the only way to replace blood
quickly
Transfused blood must be of the same blood
group
ABO Blood Group
Rh Blood Groups
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Named because of the presence or
absence of one of eight Rh antigens
(agglutinogen D)
Most Americans are Rh+
Problems can occur in mixing Rh+ blood
into a body with Rh– blood
Rh factor is named because it was
discovered in the Rhesus monkey
Rh Dangers During Pregnancy
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Danger is only when the mother is Rh– and the
father is Rh+, and the child inherits the Rh+ factor
The mismatch of an Rh– mother carrying an Rh+
baby can cause problems for the unborn child
 The first pregnancy usually proceeds without
problems
 The immune system is sensitized after the first
pregnancy
 In a second pregnancy, the mother’s immune
system produces antibodies to attack the Rh+
blood (hemolytic disease of the newborn