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PowerPoint® Lecture Slides
prepared by
Barbara Heard,
Atlantic Cape Community
Ninth Edition
College
Human Anatomy & Physiology
CHAPTER
17
Blood
© Annie Leibovitz/Contact Press Images
© 2013 Pearson Education, Inc.
Blood Composition
• Blood
– Fluid connective tissue
– Plasma – non-living fluid matrix
– Formed elements – living blood "cells"
suspended in plasma
• Erythrocytes (red blood cells, or RBCs)
• Leukocytes (white blood cells, or WBCs)
• Platelets
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Figure 17.1 The major components of whole blood.
Slide 4
Formed
elements
1 Withdraw blood
and place in tube.
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2 Centrifuge the
blood sample.
Plasma
• 55% of whole blood
• Least dense component
Buffy coat
• Leukocytes and platelets
• <1% of whole blood
Erythrocytes
• 45% of whole blood
(hematocrit)
• Most dense component
Functions of Blood
• Functions include
– Distributing substances
– Regulating blood levels of substances
– Protection
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Distribution Functions
• Delivering O2 and nutrients to body cells
• Transporting metabolic wastes to lungs
and kidneys for elimination
• Transporting hormones from endocrine
organs to target organs
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Regulation Functions
• Maintaining body temperature by
absorbing and distributing heat
• Maintaining normal pH using buffers;
alkaline reserve of bicarbonate ions
• Maintaining adequate fluid volume in
circulatory system
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Protection Functions
• Preventing blood loss
– Plasma proteins and platelets initiate clot
formation
• Preventing infection
– Antibodies
– Complement proteins
– WBCs
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Blood Plasma
• 90% water
• Over 100 dissolved solutes
– Nutrients, gases, hormones, wastes, proteins,
inorganic ions
– Plasma proteins most abundant solutes
• Remain in blood; not taken up by cells
• Proteins produced mostly by liver
• 60% albumin; 36% globulins; 4% fibrinogen
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Table 17.1 Composition of Plasma (1 of 2)
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Table 17.1 Composition of Plasma (2 of 2)
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Formed Elements
•
•
•
•
Only WBCs are complete cells
RBCs have no nuclei or other organelles
Platelets are cell fragments
Most formed elements survive in
bloodstream only few days
• Most blood cells originate in bone marrow
and do not divide
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Figure 17.2 Photomicrograph of a human blood smear stained with Wright's stain.
Platelets
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Neutrophils
Erythrocytes
Lymphocyte
Monocyte
Figure 17.3 Structure of erythrocytes (red blood cells).
2.5 µm
Side view (cut)
7.5 µm
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Top view
Erythrocytes
• Structural characteristics contribute to gas
transport
– Biconcave shape—huge surface area relative
to volume
– >97% hemoglobin (not counting water)
– No mitochondria; ATP production anaerobic;
do not consume O2 they transport
• Superb example of complementarity of
structure and function
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Figure 17.4 Structure of hemoglobin.
 Globin chains
Heme
group
 Globin chains
Hemoglobin consists of globin (two alpha and two beta
polypeptide chains) and four heme groups.
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Iron-containing heme pigment.
Hematopoiesis
• Blood cell formation in red bone marrow
– Composed of reticular connective tissue and
blood sinusoids
• In adult, found in axial skeleton, girdles,
and proximal epiphyses of humerus and
femur
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Figure 17.5 Erythropoiesis: formation of red blood cells.
Stem cell
Committed cell
Developmental pathway
Phase 1
Ribosome synthesis
Hematopoietic stem
cell (hemocytoblast)
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Proerythroblast
Basophilic
erythroblast
Phase 2
Hemoglobin accumulation
Polychromatic
erythroblast
Phase 3
Ejection of nucleus
Orthochromatic
erythroblast
Reticulocyte Erythrocyte
Regulation of Erythropoiesis
•
•
•
•
Too few RBCs leads to tissue hypoxia
Too many RBCs increases blood viscosity
> 2 million RBCs made per second
Balance between RBC production and
destruction depends on
– Hormonal controls
– Adequate supplies of iron, amino acids, and B
vitamins
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Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.
Slide 1
Homeostasis: Normal blood oxygen levels
1 Stimulus:
Hypoxia
(inadequate O2
delivery) due to
• Decreased
RBC count
• Decreased amount
of hemoglobin
• Decreased
availability of O2
5 O2-carrying
ability of blood
rises.
4 Enhanced
erythropoiesis
increases RBC count.
3 Erythropoietin
stimulates red
bone marrow.
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2 Kidney (and liver to
a smaller extent)
releases
erythropoietin.
Dietary Requirements for Erythropoiesis
• Nutrients—amino acids, lipids, and
carbohydrates
• Iron
– Available from diet
– 65% in Hb; rest in liver, spleen, and bone marrow
– Free iron ions toxic
• Stored in cells as ferritin and hemosiderin
• Transported in blood bound to protein transferrin
• Vitamin B12 and folic acid necessary for DNA
synthesis for rapidly dividing cells (developing
RBCs)
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Fate and Destruction of Erythrocytes
• Life span: 100–120 days
– No protein synthesis, growth, division
• Old RBCs become fragile; Hb begins to
degenerate
• Get trapped in smaller circulatory channels
especially in spleen
• Macrophages engulf dying RBCs in spleen
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Fate and Destruction of Erythrocytes
• Heme and globin are separated
– Iron salvaged for reuse
– Heme degraded to yellow pigment bilirubin
– Liver secretes bilirubin (in bile) into intestines
• Degraded to pigment urobilinogen
• Pigment leaves body in feces as stercobilin
– Globin metabolized into amino acids
• Released into circulation
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Figure 17.7 Life cycle of red blood cells.
Slide 1
1 Low O2 levels in blood stimulate
kidneys to produce erythropoietin.
2 Erythropoietin levels rise in blood.
3 Erythropoietin and necessary
raw materials in blood promote
erythropoiesis in red bone marrow.
4 New erythrocytes
enter bloodstream;
function about 120
days.
5 Aged and damaged
red blood cells are engulfed
by macrophages of spleen,
liver, and bone marrow; the
hemoglobin is broken down.
Hemoglobin
Heme
Bilirubin is
picked up
by the liver.
Globin
Iron is stored
as ferritin or
hemosiderin.
Amino
acids
Iron is bound to transferrin
and released to blood
from liver as needed
for erythropoiesis.
Bilirubin is secreted into
intestine in bile where
it is metabolized to
stercobilin by bacteria.
Circulation
6 Raw materials are
made available in blood
for erythrocyte synthesis.
Stercobilin
is excreted
in feces.
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Food nutrients
(amino acids, Fe,
B12, and folic acid)
are absorbed from
intestine and enter
blood.
Erythrocyte Disorders
• Anemia
– Blood has abnormally low O2-carrying
capacity
– Sign rather than disease itself
– Blood O2 levels cannot support normal
metabolism
– Accompanied by fatigue, pallor, shortness of
breath, and chills
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Causes of Anemia: Blood Loss
• Hemorrhagic anemia
– Blood loss rapid (e.g., stab wound)
– Treated by blood replacement
• Chronic hemorrhagic anemia
– Slight but persistent blood loss
• Hemorrhoids, bleeding ulcer
– Primary problem treated
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Causes of Anemia: Low RBC Production
• Iron-deficiency anemia
– Caused by hemorrhagic anemia, low iron
intake, or impaired absorption
– Microcytic, hypochromic RBCs
– Iron supplements to treat
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Causes of Anemia: Low RBC Production
• Pernicious anemia
– Autoimmune disease - destroys stomach
mucosa
– Lack of intrinsic factor needed to absorb B12
• Deficiency of vitamin B12
– RBCs cannot divide  macrocytes
– Treated with B12 injections or nasal gel
– Also caused by low dietary B12 (vegetarians)
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Causes of Anemia: Low RBC Production
• Aplastic anemia
– Destruction or inhibition of red marrow by
drugs, chemicals, radiation, viruses
– Usually cause unknown
– All cell lines affected
• Anemia; clotting and immunity defects
– Treated short-term with transfusions; longterm with transplanted stem cells
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Causes of Anemia: High RBC Destruction
• Hemolytic anemias
– Premature RBC lysis
– Caused by
• Hb abnormalities
• Incompatible transfusions
• Infections
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Causes of Anemia: High RBC Destruction
• Usually genetic basis for abnormal Hb
• Globin abnormal
– Fragile RBCs lyse prematurely
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Causes of Anemia: High RBC Destruction
• Thalassemias
– Typically Mediterranean ancestry
– One globin chain absent or faulty
– RBCs thin, delicate, deficient in Hb
– Many subtypes
• Severity from mild to severe
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Causes of Anemia: High RBC Destruction
• Sickle-cell anemia
– Hemoglobin S
• One amino acid wrong in a globin beta chain
– RBCs crescent shaped when unload O2 or
blood O2 low
– RBCs rupture easily and block small vessels
• Poor O2 delivery; pain
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Sickle-cell Anemia
• Black people of African malarial belt and
descendants
• Malaria
– Kills 1 million each year
• Sickle-cell gene
– Two copies  Sickle-cell anemia
– One copy  Sickle-cell trait; milder disease;
better chance to survive malaria
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Figure 17.8 Sickle-cell anemia.
Val His Leu Thr Pro Glu Glu …
1
2
3
4
5
6
7
146
Normal erythrocyte has normal
hemoglobin amino acid sequence
in the beta chain.
Val His Leu Thr Pro Val Glu …
1
2
3
4
5
6
7
146
Sickled erythrocyte results from a
single amino acid change in the
beta chain of hemoglobin.
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Leukocytes
• Make up <1% of total blood volume
– 4,800 – 10,800 WBCs/μl blood
• Function in defense against disease
– Can leave capillaries via diapedesis
– Move through tissue spaces by ameboid
motion and positive chemotaxis
• Leukocytosis: WBC count over
11,000/mm3
– Normal response to infection
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Leukocytes: Two Categories
• Granulocytes – Visible cytoplasmic
granules
– Neutrophils, eosinophils, basophils
• Agranulocytes – No visible cytoplasmic
granules
– Lymphocytes, monocytes
• Decreasing abundance in blood
– Never let monkeys eat bananas
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Lymphocytes
• Second most numerous WBC
• Large, dark-purple, circular nuclei with thin
rim of blue cytoplasm
• Mostly in lymphoid tissue (e.g., lymph
nodes, spleen); few circulate in blood
• Crucial to immunity
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Lymphocytes
• Two types
– T lymphocytes (T cells) act against virusinfected cells and tumor cells
– B lymphocytes (B cells) give rise to plasma
cells, which produce antibodies
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Figure 17.11 Leukocyte formation.
Stem cells
Hematopoietic stem cell
(hemocytoblast)
Lymphoid stem cell
Myeloid stem cell
Committed
cells
Myeloblast
Developmental
Promyelocyte
pathway
Eosinophilic
myelocyte
Myeloblast
Myeloblast
Monoblast
Promyelocyte
Promyelocyte
Promonocyte
Basophilic
myelocyte
Neutrophilic
myelocyte
Eosinophilic
band cells
Basophilic
band cells
Neutrophilic
band cells
(b)
Basophils
Neutrophils
(c)
Monocytes
(d)
B lymphocytes T lymphocytes
(e)
(f)
Some become
Some become
Macrophages (tissues) Plasma cells
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T lymphocyte
precursor
Agranular
leukocytes
Granular
leukocytes
Eosinophils
(a)
B lymphocyte
precursor
Some become
Effector T cells
Leukocyte disorders
• Leukopenia
– Abnormally low WBC count—drug induced
• Leukemias – all fatal if untreated
–
–
–
–
Cancer  overproduction of abnormal WBCs
Named according to abnormal WBC clone involved
Myeloid leukemia involves myeloblast descendants
Lymphocytic leukemia involves lymphocytes
• Acute leukemia derives from stem cells;
primarily affects children
• Chronic leukemia more prevalent in older people
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Leukemia
• Cancerous leukocytes fill red bone marrow
– Other lines crowded out  anemia; bleeding
• Immature nonfunctional WBCs in
bloodstream
• Death from internal hemorrhage;
overwhelming infections
• Treatments
– Irradiation, antileukemic drugs; stem cell
transplants
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Table 17.2 Summary of Formed Elements of the Blood (1 of 2)
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Table 17.2 Summary of Formed Elements of the Blood (2 of 2)
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Hemostasis
• Fast series of reactions for stoppage of
bleeding
• Requires clotting factors, and
substances released by platelets and
injured tissues
• Three steps
1. Vascular spasm
2. Platelet plug formation
3. Coagulation (blood clotting)
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Hemostasis: Vascular Spasm
• Vasoconstriction of damaged blood vessel
• Triggers
– Direct injury to vascular smooth muscle
– Chemicals released by endothelial cells and
platelets
– Pain reflexes
• Most effective in smaller blood vessels
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Hemostasis: Platelet Plug Formation
• Positive feedback cycle
• Damaged endothelium exposes collagen
fibers
– Platelets stick to collagen fibers via plasma
protein von Willebrand factor
– Swell, become spiked and sticky, and release
chemical messengers
• ADP causes more platelets to stick and release
their contents
• Serotonin and thromboxane A2 enhance vascular
spasm and platelet aggregation
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Hemostasis: Coagulation
• Reinforces platelet plug with fibrin threads
• Blood transformed from liquid to gel
• Series of reactions using clotting factors
(procoagulants)
– # I – XIII; most plasma proteins
– Vitamin K needed to synthesize 4 of them
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Figure 17.13 Events of hemostasis.
Slide 1
Step 1 Vascular spasm
• Smooth muscle contracts,
causing vasoconstriction.
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Collagen
fibers
Step 2 Platelet plug
formation
• Injury to lining of vessel
exposes collagen fibers;
platelets adhere.
Platelets
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
Fibrin
Step 3 Coagulation
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (1 of 2)
Phase 1
Intrinsic pathway
Vessel endothelium
ruptures, exposing
underlying tissues
(e.g., collagen)
Extrinsic pathway
Tissue cell trauma
exposes blood to
Platelets cling and their
surfaces provide sites for
mobilization of factors
Tissue factor (TF)
XII
Ca2+
XIIa
VII
XI
XIa
VIIa
Ca2+
IX
IXa
PF3
released by
aggregated
platelets
VIII
VIIIa
TF/VIIa complex
IXa/VIIIa complex
X
Xa
Ca2+
PF3
Va
Prothrombin
activator
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V
Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (2 of 2)
Phase 2
Prothrombin (II)
Thrombin (IIa)
Phase 3
Fibrinogen (I)
(soluble)
Ca2+
Fibrin
(insoluble
polymer)
XIII
XIIIa
Cross-linked
fibrin mesh
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Figure 17.15 Scanning electron micrograph of erythrocytes trapped in a fibrin mesh.
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Clot Retraction
• Stabilizes clot
• Actin and myosin in platelets contract
within 30–60 minutes
• Contraction pulls on fibrin strands,
squeezing serum from clot
• Draws ruptured blood vessel edges
together
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Transfusions
• Whole-blood transfusions used when
blood loss rapid and substantial
• Packed red cells (plasma and WBCs
removed) transfused to restore oxygencarrying capacity
• Transfusion of incompatible blood can be
fatal
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Human Blood Groups
• RBC membranes bear 30 types of glycoprotein
antigens
– Anything perceived as foreign; generates an immune
response
– Promoters of agglutination; called agglutinogens
• Mismatched transfused blood perceived as
foreign
– May be agglutinated and destroyed; can be fatal
• Presence or absence of each antigen is used to
classify blood cells into different groups
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ABO Blood Groups
• Types A, B, AB, and O
• Based on presence or absence of two
agglutinogens (A and B) on surface of
RBCs
• Blood may contain preformed anti-A or
anti-B antibodies (agglutinins)
– Act against transfused RBCs with ABO
antigens not present on recipient's RBCs
• Anti-A or anti-B form in blood at about
2 months of age; adult levels by 8-10
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Table 17.4 ABO Blood Groups
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Rh Blood Groups
• 52 named Rh agglutinogens (Rh factors)
• C, D, and E are most common
• Rh+ indicates presence of D antigen
– 85% Americans Rh+
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Transfusions
• Type O universal donor
– No A or B antigens
• Type AB universal recipient
– No anti-A or anti-B antibodies
• Misleading - other agglutinogens cause
transfusion reactions
• Autologous transfusions
– Patient predonates
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Before Transfusion
• Blood typing
– Mixing RBCs with antibodies against its
agglutinogen(s) causes clumping of RBCs
– Done for ABO and for Rh factor
• Cross matching
– Mix recipient's serum with donor RBCs
– Mix recipient's RBCs with donor serum
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Figure 17.16 Blood typing of ABO blood types.
Serum
Blood being tested
Anti-B
Anti-A
Type AB (contains
agglutinogens A and B;
agglutinates with both
sera)
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)
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Restoring Blood Volume
• Death from shock may result from low
blood volume
• Volume must be replaced immediately
with
– Normal saline or multiple-electrolyte solution
(Ringer's solution) that mimics plasma
electrolyte composition
– Plasma expanders (e.g., purified human
serum albumin, hetastarch, and dextran)
• Mimic osmotic properties of albumin
• More expensive and may cause significant
complications
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