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Mount Royal College
CHAPTER
Blood
Copyright © 2010 Pearson Education, Inc.
17
Formed
elements
1 Withdraw
2 Centrifuge the
blood and place
in tube.
blood sample.
Plasma
• 55% of whole blood
• Least dense component
Buffy coat
• Leukocytes and platelets
• <1% of whole blood
Erythrocytes
• 45% of whole blood
• Most dense
component
• Hematocrit
• Percent of blood volume that is RBCs
• 47% ± 5% for males
• 42% ± 5% for females
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Figure 17.1
Physical Characteristics and Volume
• Sticky, opaque fluid
• Color scarlet to dark red
• pH 7.35–7.45
• 38C
• ~8% of body weight
• Average volume: 5–6 L for males, and 4–5
L for females
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Functions of Blood
1. Distribution of
•
O2 and nutrients to body cells
•
Metabolic wastes to the lungs and kidneys
for elimination
•
Hormones from endocrine organs to target
organs
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Functions of Blood
2. Regulation of
•
Body temperature by absorbing and
distributing heat
•
Normal pH using buffers
•
Adequate fluid volume in the circulatory
system
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Functions of Blood
3. Protection against
•
Blood loss
•
•
Plasma proteins and platelets initiate clot
formation
Infection
•
Antibodies
•
Complement proteins (small proteins that amplify
other immune cells ability to kill pathogens)
•
WBCs defend against foreign invaders
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Blood Composition
• Blood: a fluid connective tissue composed of
• Plasma
• Formed elements
• Erythrocytes (red blood cells, or RBCs)
• Leukocytes (white blood cells, or WBCs)
• Platelets
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Blood Plasma
• 90% water
• Proteins
• mostly produced by the liver
• 60% albumin
• 36% globulins
• 4% fibrinogen
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Blood Plasma
• Nitrogenous by-products of metabolism—
lactic acid, urea, creatinine
• Nutrients—glucose, carbohydrates, amino
acids
• Electrolytes—Na+, K+, Ca2+, Cl–, HCO3–
• Respiratory gases—O2 and CO2
• Hormones
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Formed Elements
(WBC, RBC, platelets)
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Formed Elements
• Only WBCs are complete cells
• RBCs have no nuclei or organelles
• Platelets are cell fragments
• Most formed elements survive in the
bloodstream for only a few days
• Most blood cells originate in bone marrow and
do not divide
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Platelets
Neutrophils
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Erythrocytes
Monocyte
Lymphocyte
Figure 17.2
RBCs or Erythrocytes
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Erythrocytes
• Biconcave discs, anucleate, essentially no
organelles
• Filled with hemoglobin (Hb) for gas transport
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2.5 µm
Side view (cut)
7.5 µm
Top view
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Figure 17.3
Erythrocytes
• Structural characteristics contribute to gas
transport
• Biconcave shape—huge surface area relative
to volume
• >97% hemoglobin (not counting water)
• No mitochondria; ATP production is anaerobic;
no O2 is used in generation of ATP
• A great example of how structure and function
work together!
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Erythrocyte Function
• Hemoglobin structure
• Protein globin: two alpha and two beta chains
• Heme pigment bonded to each globin chain (4)
• Iron atom in each heme can bind to one O2
molecule; binds reversibly
• Each Hb molecule can transport four O2
• Normal Hb: 12-16 in women, 13-18 in men
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b Globin chains
Heme
group
a Globin chains
(a) Hemoglobin consists of globin (two
alpha and two beta polypeptide
chains) and four heme groups.
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(b) Iron-containing heme pigment.
Figure 17.4
Hemoglobin (Hb)
• O2 loading in the lungs
• Produces oxyhemoglobin (ruby red)
• O2 unloading in the tissues
• Produces deoxyhemoglobin or reduced
hemoglobin (dark red)
• CO2 loading in the tissues
• Produces carbaminohemoglobin (carries 20%
of CO2 in the blood)
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Hematopoiesis
• Hematopoiesis (hemopoiesis): blood cell
formation
• Formed in red marrow
• Red marrow is found mainly in the flat bones,
such as pelvis, sternum, cranium, ribs,
vertebrae, and scapula. Also in the spongy
epiphyseal plates of long bones like the femur
and humerus.
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Stem cell
Committed
cell
Developmental pathway
Proerythroblast
Early
Late
erythroblast erythroblast
Hemocytoblast
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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
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Hormonal Control of Erythropoiesis
• Erythropoietin (EPO)
• Direct stimulus for erythropoiesis
• Released by the kidneys in response to
hypoxia
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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)
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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
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Homeostasis: Normal blood oxygen levels
1 Stimulus:
Hypoxia (low blood
O2- carrying ability)
due to
• Decreased
RBC count
• Decreased amount
of hemoglobin
• Decreased
availability of O2
5 O2- carrying
ability of blood
increases.
4 Enhanced
erythropoiesis
increases RBC
count.
2 Kidney (and liver to
3 Erythropoietin
a smaller extent)
releases
erythropoietin.
stimulates red
bone marrow.
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Figure 17.6, step 5
Dietary Requirements for Erythropoiesis
• Nutrients—amino acids, lipids, and carbohydrates
• Iron
• Stored in Hb (65%), the liver, spleen, and bone
marrow
• Stored in cells as ferritin and hemosiderin
• Vitamin B12 and folic acid—necessary for DNA
synthesis for cell division
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Fate and Destruction of Erythrocytes
• Life span: 100–120 days
• Old RBCs become fragile, and Hb begins to
degenerate
• Macrophages engulf dying RBCs in the
spleen
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1 Low O2 levels in blood stimulate
kidneys to produce erythropoietin.
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Figure 17.7, step 1
1 Low O2 levels in blood stimulate
kidneys to produce erythropoietin.
2 Erythropoietin levels rise
in blood.
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Figure 17.7, step 2
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.
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Figure 17.7, step 3
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.
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Figure 17.7, step 4
Fate and Destruction of Erythrocytes
• Heme and globin are separated
• Iron is salvaged for reuse
• Heme is degraded to yellow the pigment
bilirubin
• Liver secretes bilirubin (in bile) into the
intestines
• Degraded pigment leaves the body in feces as
stercobilin
• Globin is metabolized into amino acids
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5 Aged and damaged red
blood cells are engulfed by
macrophages of liver,
spleen, and bone
marrow; the
Bilirubin
hemoglobin is
broken down.
Hemoglobin
Heme
Globin
Amino
Iron stored
acids
as ferritin,
hemosiderin
Bilirubin is picked up from blood
by liver, secreted into intestine in
bile, metabolized to stercobilin by
bacteria, and excreted in feces.
Circulation
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Figure 17.7, step 5
5 Aged and damaged red
blood cells are engulfed by
macrophages of liver,
spleen, and bone
marrow; the
Bilirubin
hemoglobin is
broken down.
Hemoglobin
Heme
Globin
Amino
Iron stored
acids
as ferritin,
hemosiderin
Iron is bound to
transferrin and released
to blood from liver as
needed for erythropoiesis.
Bilirubin is picked up from blood
by liver, secreted into intestine in
bile, metabolized to stercobilin by
bacteria, and excreted in feces.
Circulation
Food nutrients,
including amino acids,
Fe, B12, and folic acid,
are absorbed from
intestine and enter
blood.
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6 Raw materials are
made available in blood
for erythrocyte synthesis.
Figure 17.7, step 6
1 Low O levels in blood stimulate
2
kidneys to produce erythropoietin.
2 Erythropoietin levels rise
in blood.
3 Erythropoietin and necessary
raw materials in blood promote
erythropoiesis in red bone marrow.
5 Aged and damaged
red blood cells are
engulfed by macrophages
of liver, spleen, and bone
marrow; the hemoglobin Hemoglobin
is broken down.
Heme
Bilirubin
4 New erythrocytes
enter bloodstream;
function about 120 days.
Globin
Amino
Iron stored
acids
as ferritin,
hemosiderin
Iron is bound to
transferrin and released
to blood from liver as
needed for erythropoiesis.
Bilirubin is picked up from blood
by liver, secreted into intestine in
bile, metabolized to stercobilin by
bacteria, and excreted in feces.
Circulation
Food nutrients,
including amino acids,
Fe, B12, and folic acid,
are absorbed from
intestine and enter
blood.
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6 Raw materials are
made available in blood
for erythrocyte synthesis.
Figure 17.7
Erythrocyte Disorders
• Anemia: blood has abnormally low O2carrying capacity
• A sign rather than a disease itself
• Accompanied by fatigue, paleness, shortness
of breath, and chills
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Causes of Anemia
1. Insufficient erythrocytes
•
Hemorrhagic anemia: acute or chronic loss
of blood
•
Hemolytic anemia: RBCs rupture
prematurely
•
Aplastic anemia: destruction or inhibition of
red bone marrow
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Causes of Anemia
2. Low hemoglobin content
• Iron-deficiency anemia
• Secondary result of hemorrhagic anemia or
• Inadequate intake of iron-containing foods
or
• Impaired iron absorption
• Heavy menstruation
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Causes of Anemia
• Pernicious anemia
• Deficiency of vitamin B12
• Lack of intrinsic factor needed for absorption
of B12
• Treated by intramuscular injection of B12 or
application of Nascobal
• Common in elderly and those with GI
disorders that cause malabsorption, like
Crohn’s, IBD, etc.
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Causes of Anemia
3. Abnormal hemoglobin
• Thalassemias
• Absent or faulty globin chain
• RBCs are thin, delicate, and deficient in
hemoglobin
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Causes of Anemia
• Sickle-cell anemia
• Defective gene codes for abnormal
hemoglobin (HbS)
• Causes RBCs to become sickle shaped in
low-oxygen situations
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(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
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Figure 17.8
Erythrocyte Disorders
• Polycythemia: excess of RBCs that increase
blood viscosity
• Results from:
• Polycythemia vera—bone marrow cancer
• Secondary polycythemia—when less O2 is
available (high altitude) or when EPO
production increases
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Leukocytes or WBCs
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Leukocytes
• Make up <1% of total blood volume
• Can leave capillaries via diapedesis
• Move through tissue spaces by ameboid
motion and positive chemotaxis (toward a
chemical stimulus)
• Normal range: 4-11,000/mm3
• Leukocytosis: WBC count over 11,000/mm3
• Normal response to bacterial or viral invasion
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Differential
WBC count
(All total 4800 –
10,800/l)
Formed
elements
Platelets
Leukocytes
Granulocytes
Neutrophils (50 – 70%)
Eosinophils (2 – 4%)
Basophils (0.5 – 1%)
Erythrocytes
Agranulocytes
Lymphocytes (25 – 45%)
Monocytes (3 – 8%)
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Figure 17.9
Granulocytes
• Granulocytes: neutrophils, eosinophils, and
basophils
• Cytoplasmic granules stain specifically with
Wright’s stain
• Larger and shorter-lived than RBCs
• Lobed nuclei
• Phagocytic
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Neutrophils
• Most numerous WBCs
• Aka polymorphonuclear leukocytes (PMNs)
• Granules contain hydrolytic enzymes or
defensins
• Very phagocytic—“bacteria slayers”
• THE MARINES “FIRST ONES IN”
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Eosinophils
• Red to crimson (acidophilic) coarse,
lysosome-like granules
• Allergies and digest parasitic worms that are
too large to be phagocytized
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Basophils
• Rarest WBCs
• Large, purplish-black (basophilic) granules
contain histamine
• Histamine: an inflammatory chemical that acts
as a vasodilator and attracts other WBCs to
inflamed sites
• Are functionally similar to mast cells
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(a) Neutrophil;
multilobed
nucleus
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(b) Eosinophil;
bilobed nucleus,
red cytoplasmic
granules
(c) Basophil;
bilobed nucleus,
purplish-black
cytoplasmic
granules
Figure 17.10 (a-c)
Agranulocytes
• Agranulocytes: lymphocytes and monocytes
• Lack visible cytoplasmic granules
• Have spherical or kidney-shaped nuclei
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Lymphocytes
• Large, dark-purple, circular nuclei with a thin
rim of blue cytoplasm
• Mostly in lymphoid tissue; few circulate in the
blood
• Crucial to immunity
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Lymphocytes
• Two types
• T cells act against virus-infected cells and
tumor cells (cell mediated immune response)
• B cells give rise to plasma cells, which
produce antibodies (humoral immune
response)
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Monocytes
• The largest leukocytes
• Abundant pale-blue cytoplasm
• Dark purple-staining, U- or kidney-shaped
nuclei
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Monocytes
• Leave circulation, enter tissues, and
differentiate into macrophages
• Actively phagocytic cells; crucial against
viruses, intracellular bacterial parasites, and
chronic infections
• Activate lymphocytes to mount an immune
response
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(d) Small
lymphocyte;
large spherical
nucleus
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(e) Monocyte;
kidney-shaped
nucleus
Figure 17.10d, e
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Table 17.2 (1 of 2)
Leukopoiesis
• Production of WBCs
• Stimulated by chemical messengers from
bone marrow and mature WBCs
• Interleukins (e.g., IL-1, IL-2)
• All leukocytes originate from hemocytoblasts
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Stem cells
Hemocytoblast
Lymphoid stem cell
Myeloid stem cell
Committed
cells
Myeloblast
Developmental Promyelocyte
pathway
Myeloblast
Myeloblast
Monoblast
Lymphoblast
Promyelocyte Promyelocyte Promonocyte
Eosinophilic Basophilic
myelocyte
myelocyte
Neutrophilic
myelocyte
Eosinophilic Basophilic
band cells
band cells
Neutrophilic
band cells
Monocytes
Eosinophils Basophils Neutrophils
(a)
(b)
(c)
(d)
Granular leukocytes
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Prolymphocyte
Lymphocytes
(e)
Agranular leukocytes
Some become
Some
become
Figure 17.11
Leukocyte Disorders
• Leukopenia
• Abnormally low WBC count—drug/toxin induced
• Leukemias
• 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
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Leukemia
• 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
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Platelets
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Platelets
• Form a temporary platelet plug that helps seal breaks
in blood vessels
• Circulating platelets are kept inactive and mobile by
NO (nitric oxide) and prostacyclin from endothelial
cells of blood vessels
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Stem cell
Developmental pathway
Hemocytoblast
Promegakaryocyte
Megakaryoblast
Megakaryocyte
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Platelets
Figure 17.12
Hemostasis
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Hemostasis
•
Fast series of reactions for stoppage of
bleeding
1. Vascular spasm
2. Platelet plug formation
3. Coagulation (blood clotting)
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Vascular Spasm
• Vasoconstriction of damaged blood vessel
• Triggers
• Direct injury
• Chemicals released by endothelial cells and
platelets
• Pain reflexes
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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
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Step 3 Coagulation
• Fibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
Figure 17.13
Coagulation
• A set of reactions in which blood is
transformed from a liquid to a gel
• Reinforces the platelet plug with fibrin
threads
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Coagulation
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Coagulation
•
Three phases of coagulation
1. Prothrombin activator is formed (intrinsic and
extrinsic pathways)
2. Prothrombin is converted into thrombin
3. Thrombin catalyzes the joining of fibrinogen
to form a fibrin mesh
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Phase 1
Intrinsic pathway
Vessel endothelium ruptures,
exposing underlying tissues
(e.g., collagen)
Platelets cling and their
surfaces provide sites for
mobilization of factors
XII
XIIa
Extrinsic pathway
Tissue cell trauma
exposes blood to
Tissue factor (TF)
Ca2+
VII
XI
XIa
VIIa
Ca2+
IX
PF3
released by
aggregated
platelets
IXa
VIII
VIIIa
TF/VIIa complex
IXa/VIIIa complex
X
Xa
Ca2+
PF3
V
Va
Prothrombin
activator
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Figure 17.14 (1 of 2)
Phase 2
Prothrombin
activator
Prothrombin (II)
Thrombin (IIa)
Phase 3
Fibrinogen (I)
(soluble)
Ca2+
Fibrin
(insoluble
polymer)
XIII
XIIIa
Cross-linked
fibrin mesh
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Figure 17.14 (2 of 2)
CLOTTING PATHWAYS
Intrinsic Pathway:
Blood trauma (turbulence and viscosity) or
collagen and blood contact.
Measured by:
PTT
Drugs:
Heparin
Measured
by PT/INR
Drugs: Warfarin,
ASA, Vitamin-E,
EFA’s
Extrinsic
Pathway:
Damage outside of blood
Factorsvessels.
2-7-9-10
PROTHROMBIN
ACTIVATOR made up of V&X:
Started by X alone and V becomes active with +
feedback
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Figure 17.15
Clot Retraction
• Actin and myosin in platelets contract within
30–60 minutes
• Platelets pull on the fibrin strands, squeezing
serum from the clot
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Clot Repair
• 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
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Fibrinolysis
• 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
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Factors Preventing Undesirable Clotting
• Platelet adhesion is prevented by
• Smooth endothelial lining of blood vessels
• Antithrombic substances nitric oxide and
prostacyclin secreted by endothelial cells
• Vitamin E quinine, which acts as a potent
anticoagulant
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Disorders of Hemostasis
• Thromboembolytic disorders: undesirable clot
formation
• Bleeding disorders: abnormalities that prevent
normal clot formation
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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
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Thromboembolytic 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
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Disseminated Intravascular Coagulation
(DIC)
• Widespread clotting blocks intact blood
vessels
• Severe bleeding occurs because residual
blood unable to clot
• Most common in pregnancy, septicemia, or
incompatible blood transfusions
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Bleeding Disorders
• Thrombocytopenia: deficient number of
circulating platelets
• Petechiae appear due to spontaneous,
widespread hemorrhage
• 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
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Bleeding Disorders
• 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
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Bleeding Disorders
• Hemophilias include several similar hereditary
bleeding disorders
• Hemophilia A: most common type (77% of all cases);
due to a deficiency of factor VIII
• Hemophilia B: deficiency of factor IX
• Hemophilia C: mild type; deficiency of factor XI
• Symptoms include prolonged bleeding, especially
into joint cavities
• Treated with plasma transfusions and injection of
missing factors
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Transfusions
• Whole-blood transfusions are used when
blood loss is substantial
• Packed red cells (plasma removed) are used
to restore oxygen-carrying capacity
• Transfusion of incompatible blood can be fatal
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Blood Types
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Blood Groups
• Humans have 30 varieties of naturally
occurring RBC antigens
• Antigens of the ABO and Rh blood groups
cause vigorous transfusion reactions
• Other blood groups (MNS, Duffy, Kell, and
Lewis) are usually weak agglutinogens
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ABO Blood Groups
• Types A, B, AB, and O
• Based on the presence or absence of two
agglutinogens (A and B) on the surface of the
RBCs
• Blood may contain anti-A or anti-B antibodies
(agglutinins) that act against transfused RBCs
with ABO antigens not normally present
• Anti-A or anti-B form in the blood at about
2 months of age
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Table 17.4
Rh Blood Groups
• There are 45 different Rh agglutinogens (Rh
factors)
• C, D, and E are most common
• Rh+ indicates presence of D
• Rh+ = 85% of the population
• Rh- = 15% of the population
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Rh Blood Groups
• Anti-Rh antibodies are not spontaneously
formed in Rh– individuals
• Anti-Rh antibodies form if an Rh– individual
receives Rh+ blood
• A second exposure to Rh+ blood will result in
a typical transfusion reaction
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Homeostatic Imbalance: Hemolytic Disease
of the Newborn
• Also called erythroblastosis fetalis
• Rh– mother becomes sensitized when
exposure to Rh+ blood causes her body to
synthesize anti-Rh antibodies
• Anti-Rh antibodies cross the placenta and
destroy the RBCs of an Rh+ baby
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Homeostatic Imbalance: Hemolytic Disease
of the Newborn
• The baby can be treated with prebirth
transfusions and exchange transfusions after
birth
• RhoGAM serum containing anti-Rh can
prevent the Rh– mother from becoming
sensitized
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ABO Blood Typing
Blood
Type
Being
Tested
RBC
Agglutinogens
Serum
Reaction
Anti-A Anti-B
AB
A and B
+
+
B
B
–
+
A
A
+
–
O
None
–
–
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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)
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Figure 17.16
Restoring Blood Volume
• Death from shock may result from low blood volume
• Volume must be replaced immediately with
• Normal saline or multiple-electrolyte 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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Diagnostic Blood Tests
• Hematocrit
• Blood glucose tests
• Microscopic examination reveals variations in
size and shape of RBCs, indications of
anemias
• RBCs too big = macrocytic anemia (B12/folic
acid deficiency, etc.)
• RBCs too small = microcytic anemia (iron
deficiency, thalassemia, etc.)
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Diagnostic Blood Tests
• Differential WBC count
• Prothrombin time (PTT) and platelet counts
assess hemostasis
• SMAC (or CMP), a blood chemistry profile
• Complete blood count (CBC)
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Developmental Aspects
• Fetal blood cells form in the fetal yolk sac,
liver, and spleen
• Red bone marrow is the primary
hematopoietic area by the seventh month
• Blood cells develop from mesenchymal cells
called blood islands
• The fetus forms HbF, which has a higher
affinity for O2 than hemoglobin A formed after
birth
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Developmental Aspects
• Blood diseases of aging
• Chronic leukemias, anemias, clotting disorders
• Usually precipitated by disorders of the heart,
blood vessels, and immune system
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QUESTIONS TO TEST
WHAT YOU NOW KNOW!!!
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Which of the following comprise a logical
sequence of vessels as blood exits the
heart?
A. Capillaries, arteries, veins
B. Veins, capillaries, arteries
C. Arteries, capillaries, veins
D. Arteries, veins, capillaries
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After centrifuging, of the listed blood
components, which contains the
components of immune function?
A. Plasma
B. Buffy coat
C. Erythrocytes
D. Hematocrit
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The major function of the most common
plasma protein, albumin, is __________.
A. maintenance of plasma osmotic pressure
B. buffering changes in plasma pH
C. fighting foreign invaders
D. both a and b
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Red blood cells are efficient oxygen
transport cells. Of the following
characteristics, which is the major
contributor to the significant oxygencarrying capacity of a red blood cell?
A. Red blood cells lack mitochondria.
B. Red blood cells don’t divide.
C. Red blood cells are biconcave discs.
D. Red blood cells contain myoglobin.
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Each hemoglobin can transport ________
oxygen atoms.
A. 4
B. 40
C. 400
D. 4000
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Oxygen binds to the _______ portion of
hemoglobin.
A. globin
B. oxyhemoglobin
C. iron atom
D. amino acid
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A patient with low iron levels would
experience which of the following
symptoms?
A. An increased white blood cell count
B. An increase in energy level
C. An increase in fatigue
D. A decreased white blood cell count
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A hematopoietic stem cell will give rise to
__________.
A. erythrocytes
B. leukocytes
C. platelets
D. all of the above
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Predict the outcome of an overdose of the
hormone erythropoietin.
A. The blood viscosity increases to levels that
may induce heart attacks or strokes.
B. The oxygen-carrying capacity remains
unchanged despite elevated red blood cell
counts.
C. Red blood cell counts remain unchanged,
but the number of reticulocytes increases.
D. Blood viscosity levels decrease while
oxygen-carrying capacity increases.
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What response would you expect after
traveling to high altitude for two weeks?
A. Blood levels of oxygen would remain
depressed for the duration.
B. A surge in iron release from the liver would
occur.
C. The kidneys would secrete elevated
amounts of erythropoietin.
D. There would be no change in blood
composition.
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If a patient has pernicious anemia, the
inability of the body to absorb vitamin B12,
the patient __________.
A. would have reduced blood iron levels
B. would have a decreased number of red
blood cells
C. would have increased levels of hemoglobin
D. would not experience any effects on red
blood cells
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Which of the following statements is true
regarding the mechanism controlling
movement of white blood cells into
damaged areas?
A. White blood cells exit the capillary and move
through the tissue spaces with cytoplasmic
extensions by following a trail of chemicals
produced by other white blood cells.
B. Capillaries break open, flooding a damaged area
with white blood cells.
C. The damaged tissues synthesize their own white
blood cells.
D. None of the statements are true.
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An elevated neutrophil count would be
indicative of ________.
A. an allergic reaction
B. a cancer
C. an acute bacterial infection
D. a parasitic infection
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Antihistamines counter the actions of which
white blood cells?
A. Neutrophils
B. Lymphocytes
C. Basophils
D. Eosinophils
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Leukemia is a general descriptor for which
of the following disorders?
A. An abnormally low white blood cell count
B. Overproduction of abnormal leukocytes
C. Elevated counts of normal neutrophils
D. Overproduction of abnormal erythrocytes
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A __________ is the progenitor of platelets.
A. thrombopoietin
B. thrombocyte
C. megakaryocyte
D. thrombocytoblast
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Why don’t platelets form plugs in
undamaged vessels?
A. Platelets aren’t formed until vessel damage
occurs.
B. Only contact of platelets with exposed
collagen fibers and von Willebrand factor
causes them to be sticky and form plugs.
C. Plugs do form, but are removed by
macrophages.
D. Platelets don’t form plugs, it is the
megakaryocytes that form the plugs.
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Activation of the extrinsic pathway of
coagulation requires exposure of the blood
to _________.
A. collagen
B. tissue factor III
C. prothrombin activator
D. serotonin
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Why doesn’t a clot fill the entire
vasculature system once it has started
forming?
A. Rapid blood flow washes away and dilutes
activated clotting factors.
B. Thrombin is inactivated by antithrombin III if
it enters the general circulation.
C. Both a and b occur.
D. Neither a nor b occurs.
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An oral heparin medication might be
prescribed for a patient who:
A. is at risk for embolism (clots that
spontaneously form and wedge in blood
vessels).
B. has thrombocytopenia.
C. is a hemophiliac.
D. has a deficiency in a clotting factor.
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Why is it possible for a person with type A
negative blood to have a negative reaction
when receiving a transfusion of whole type
O negative blood?
A. Some type O cells possess B agglutinogens on
their surface.
B. The Rh factor would cross-react.
C. Blood transfusions can only occur within the same
blood group.
D. The type O blood may have high enough levels of
anti-A antibodies that could cross-react with the
recipient’s cells.
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