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Introduction
Erythrocytes
Blood types
Leukocytes
Platelets and Hemostasis The
Control of Bleeding
18-1
Circulatory System
circulatory system consists of the heart, blood vessels
and blood
cardiovascular system refers only to the heart and
blood vessels
hematology the study of blood
functions of circulatory system
transport
O2, CO2, nutrients, wastes, hormones, and stem cells
protection
inflammation, limit spread of infection, destroy microorganisms and
cancer cells, neutralize toxins, and initiates clotting
regulation
fluid balance, stabilizes pH of ECF, and temperature control
18-2
of
18-4
Monocyte
Small
lymphocyte
Platelets
Neutrophil
Eosinophil
Small
lymphocyte
Erythrocyte
Young (band)
neutrophil
Neutrophil
Monocyte
Large
lymphocyte
Neutrophil
Basophil
Figure 18.1
18-5
Withdraw
blood
hematocrit - centrifuge
blood to separate
components
Centrifuge
1% total volume
buffy coat
Figure 18.2
Plasma
(55% of whole blood)
Erythrocytes
(45% of whole blood)
plasma
Formed
elements
globulins (antibodies)
provide immune system functions
alpha, beta and gamma globulins
fibrinogen
precursor of fibrin threads that help form blood clots
18-7
nutrients
glucose, vitamins, fats, cholesterol, phospholipids,
and minerals
18-8
Properties of Blood
viscosity - resistance of a fluid to flow, resulting
from the cohesion of its particles
whole blood 4.5 - 5.5 times as viscous as water
plasma is 2.0 times as viscous as water
important in circulatory function
18-9
kwashiorkor
children with severe protein deficiency
fed on cereals once weaned
thin arms and legs
swollen abdomen
18-10
Hemopoiesis
adult production of 400 billion platelets, 200 billion RBCs and 10
billion WBCs every day
hemopoiesis the production of blood, especially its formed
elements
hemopoietic tissues produce blood cells
yolk sac produces stem cells for first blood cells
colonize fetal bone marrow, liver, spleen and thymus
one
18-11
Erythrocytes
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Capillary
wall
Erythrocytes
Figure 18.4c
(c)
7 m
Dr. Don W. Fawcett/Visuals Unlimited
18-12
Erythrocytes (RBCs)
disc-shaped cell with thick rim
7.5 M diameter and 2.0 m thick
at rim
lose nearly all organelles during
development
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Surfaceview
lack mitochondria
7.5 m
2.0 m
(a)
Sectional view
Figure 18.4a
18-13
heme groups
Beta
Alpha
Heme
groups
(a)
Beta
Alpha
CH3
CH
C
C
C
N
C
N
CH2
CH3
CH2
HC
CH
C
Fe2+
CH2
CH3
CH
N
C
N
C
CH2
CH
COOH
C
CH2
CH3
CH2
(b)
COOH
18-15
RBC count
men 4.6-6.2 million/L; women 4-2-5.4 million/L
18-16
Pluripotent
stem cell
Colony-forming
unit (CFU)
Erythrocyte CFU
Precursor
cells
Erythroblast
Mature
cell
Reticulocyte
Erythrocyte
Figure 18.6
2.5 million RBCs are produced per second
average lifespan of about 120 days
development takes 3-5 days
reduction in cell size, increase in cell number, synthesis of hemoglobin
and loss of nucleus
18-17
Iron Metabolism
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
leaves
8 Remaining transferrin is distributed
to other organs where Fe2+ is used
to make hemoglobin, myoglobin, etc.
7 Fe2+ binds to
apoferritin
to be stored
as ferritin
Fe3+
2 Stomach acid
converts Fe3+
to Fe2+
Ferritin
Fe2+
Apoferritin
Gastroferritin
6 In liver, some transferrin
releases Fe2+ for storage
Blood plasma
5 In blood plasma,
Fe2+ binds to transferrin
Transferrin
3 Fe2+ binds to
gastroferritin
4 Gastroferritin transports
Fe2+ to small intestine and
releases it for absorption
Figure 18.7
18-18
18-19
Erythrocyte Homeostasis
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Hypoxemia
(inadequate O2 transport)
Increased
O2 transport
leaves
Increased
RBC count
Accelerated
erythropoiesis
Secretion of
erythropoietin
Stimulation of
red bone marrow
Figure 18.8
18-21
18-22
Erythrocytes Recycle/Disposal
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Amino acids
Iron
Folic acid
Vitamin B12
Erythropoiesis in
red bone marrow
Nutrient
absorption
Erythrocytes
circulate for
120 days
Small intestine
Expired erythrocytes
break up in liver and spleen
Cell fragments
phagocytized
Hemoglobin
degraded
Globin
Heme
Biliverdin
Bilirubin
Bile
Feces
Iron
Storage
Reuse
Figure 18.9
Hydrolyzed to free
amino acids
Loss by
menstruation,
injury, etc.
18-23
Erythrocyte Disorders
polycythemia - an excess of RBCs
primary polycythemia (polycythemia vera)
cancer of erythropoietic cell line in red bone
marrow
RBC count as high as 11 million/L; hematocrit 80%
secondary polycythemia
from dehydration, emphysema, high altitude, or
physical conditioning
RBC count up to 8 million/L
dangers of polycythemia
increased blood volume, pressure, viscosity
can lead to embolism, stroke or heart failure
18-24
Anemia
causes of anemia fall into three categories:
inadequate erythropoiesis or hemoglobin synthesis
kidney failure and insufficient erythropoietin
iron-deficiency anemia
inadequate vitamin B12 from poor nutrition or lack of intrinsic
factor (pernicious anemia)
hypoplastic anemia slowing of erythropoiesis
aplastic anemia - complete cessation of erythropoiesis
Anemia
anemia has three potential consequences:
tissue hypoxia and necrosis
patient is lethargic
shortness of breath upon exertion
life threatening necrosis of brain, heart, or kidney
Sickle-Cell Disease
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
7 m
Figure 18.10
Blood Types
blood types and transfusion compatibility
are a matter of interactions between
plasma proteins and erythrocytes
Karl Landsteiner discovered blood types
A, B and O in 1900
won Nobel Prize
antibodies
proteins (gamma globulins) secreted by plasma cells
agglutination
antibody molecule binding to antigens
causes clumping of red blood cells
18-29
Blood Types
RBC antigens called
agglutinogens
called antigen A and B
determined by
carbohydrate moieties
found on RBC surface
antibodies called
agglutinins
found in plasma
anti-A and anti-B
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Type O
Type B
leaves
Type A
Type AB
Key
Galactose
Fucose
N-acetylgalactosamine
Figure 18.12
18-30
ABO Group
your ABO blood type is determined by
presence or absence of antigens
(agglutinogens) on RBCs
blood type A person has A antigens
blood type B person has B antigens
blood type AB has both A and B antigens
blood type O person has neither antigen
most common - type O
rarest - type AB
18-31
Type A
Type B
Type AB
Figure 18.14
Type O
18-32
Claude Revey/Phototake
Plasma Antibodies
antibodies (agglutinins); anti-A and anti-B
appear 2-8 months after birth; at maximum
concentration at 10 yr.
antibody-A and/or antibody-B (both or none) are found in plasma
you do not form antibodies against your antigens
agglutination
each antibody can attach to several foreign antigens on several
different RBCs at the same time
Agglutination of Erythrocytes
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Antibodies
(agglutinins)
Figure 18.13
18-34
Transfusion Reaction
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Blood from
type A donor
leaves
Type B
(anti-A)
recipient
Donor RBCs
agglutinated by
recipient plasma
Agglutinated RBCs
block small vessels
Figure 18.15
18-35
universal recipient
Type AB rarest blood type
lacks plasma antibodies; no anti- A or B
18-36
Rh Group
Rh (C,D,E) agglutinogens discovered in
rhesus monkey in 1940
Rh D is the most reactive and a patient is
considered blood type Rh+ if they have D
antigen (agglutinogens) on RBCs
Rh frequencies vary among ethnic groups
18-37
prevention
RhoGAM given to pregnant Rh- women
binds fetal agglutinogens in her blood so she will
not form Anti-D antibodies
18-38
leaves
Rh mother
Rh
antigen
Second
Rh+ fetus
Rh+ fetus
Uterus
Amniotic sac
and chorion
Anti-D
antibody
Placenta
Figure 18.16
(a) First pregnancy
18-39
Leukocytes (WBCs)
least abundant formed element
5,000 to 10,000 WBCs/L
18-40
Types of Leukocytes
granulocytes
neutrophils (60-70%)-polymorphonuclear leukocytes
barely-visible granules in cytoplasm; 3 to 5 lobed nucleus
eosinophils (2-4%)
large rosy-orange granules; bilobed nucleus
basophils (<1%)
large, abundant, violet granules (obscure a large S-shaped
nucleus)
agranulocytes
lymphocytes (25-33%)
variable amounts of bluish cytoplasm (scanty to abundant);
ovoid/round, uniform dark violet nucleus
monocytes (3-8%)
largest WBC; ovoid, kidney-, or horseshoe- shaped nucleus
18-41
Granulocytes
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Neutrophils
10 m
Eosinophil
10 m
Basophil
10 m
all: Ed Reschke
Figure TA 18.1
Figure TA 18.2
Figure TA 18.3
18-42
Agranulocytes
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Lymphocyte
10 m
Monocyte
10 m
Figure TA 18.4
Figure TA 18.5
18-43
Granulocyte Functions
neutrophils - increased numbers in bacterial infections
phagocytosis of bacteria
release antimicrobial chemicals
18-44
Agranulocyte Functions
lymphocytes - increased numbers in diverse
infections and immune responses
destroy cells (cancer, foreign, and virally infected
cells)
present antigens to activate other immune cells
coordinate actions of other immune cells
secrete antibodies and provide immune memory
18-45
18-47
Leukopoiesis
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pluripotent
stem cell
Colony-forming
units (CFUs)
Mature
cells
Precursor
cells
leaves
Eosinophilic
CFU
Eosinophilic
myeloblast
Eosinophilic
promyelocyte
Eosinophilic
myelocyte
Eosinophil
Basophilic
CFU
Basophilic
myeloblast
Basophilic
promyelocyte
Basophilic
myelocyte
Basophil
Neutrophilic
CFU
Neutrophilic
myeloblast
Neutrophilic
promyelocyte
Neutrophilic
myelocyte
Neutrophil
Monocytic
CFU
Monoblast
Promonocyte
B prolymphocyte
Lymphocytic
CFU
Lymphoblast
Monocyte
B lymphocyte
T prolymphocyte
T lymphocyte
NK prolymphocyte
NK cell
Figure 18.18
18-48
Leukocyte Disorders
leukopenia - low WBC count below 5000/L
causes: radiation, poisons, infectious disease
effects: elevated risk of infection
Platelets
Monocyte
Neutrophils
Lymphocyte
Erythrocytes
(a)
(b)
75 m
Ed Reschke
18-50
Hemostasis
hemostasis the cessation of bleeding
stopping potentially fatal leaks
hemorrhage excessive bleeding
18-51
Platelets
platelets - small fragments of megakaryocyte cells
2-4 m diameter; contain granules
complex internal structure and open canalicular system
amoeboid movement and phagocytosis
Platelets
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pseudopod
Granules
Open
canalicular
system
Mitochondria
(a)
2 m
Platelets
Bloodflow
Proplatelets
RBC
WBC
Megakaryocyte
(b)
18-53
a: NIBSC/Science Photo Library/Photo Researchers, Inc.
18-54
Hemostasis
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Vasoconstriction
Platelet
plug
Platelet
Blood
clot
Vessel
injury
Collagen
fibers
Endothelial
cells
(a) Vascular spasm
(c) Coagulation
18-55
causes:
pain receptors
some directly innervate blood vessels to constrict
effects:
prompt constriction of a broken vessel
pain receptors - short duration (minutes)
smooth muscle injury - longer duration
18-56
Hemostasis - Coagulation
coagulation (clotting) last and most effective
defense against bleeding
conversion of plasma protein fibrinogen into insoluble
fibrin threads to form framework of clot
extrinsic pathway
factors released by damaged tissues begin cascade
intrinsic pathway
factors found in blood begin cascade (platelet
degranulation)
18-58
Figure 18.22
18-59
Coagulation Pathways
Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Extrinsic mechanism
Intrinsic mechanism
Factor XII
Factor XI
(active)
Damaged
perivascular
tissues
Factor IX
(active)
Thromboplastin
(factor III)
Platelets
Inactive
Inactive
Ca2+, PF3
Factor VII
Factor VIII
(active)
Inactive
Ca2+
extrinsic pathway
initiated by release of tissue
thromboplastin (factor III)
from damaged tissue
cascade to factor VII, V and X
(fewer steps)
intrinsic pathway
Factor X
(active)
Inactive
Factor III
Factor V
Ca2+
PF3
Prothrombin
activator
Prothrombin
(factor II)
Factor V
Thrombin
Factor XIII
Ca2+
Fibrinogen
(factor I)
Fibrin
Figure 18.23
Fibrin
polymer
Factor
XII
Figure 18.24
Factor
IX
Factor
VIII
Factor
X
Prothrombin
activator
Factor
XI
Thrombin
Fibrin
Completion of Coagulation
activation of factor X
leads to production of prothrombin activator
prothrombin activator
converts prothrombin to thrombin
thrombin
converts fibrinogen into fibrin
Prekallikrein
Factor
XII
Kallikrein
Plasminogen
Positive
feedback
loop
Figure 18.25
Plasmin
Fibrin
polymer
Clot dissolution
Fibrin degradation
products
18-64
thrombin dilution
by rapidly flowing blood
heart slowing in shock can result in clot formation
natural anticoagulants
heparin (from basophils and mast cells) interferes
with formation of prothrombin activator
antithrombin (from liver) deactivates thrombin
before it can act on fibrinogen
18-65
Coagulation Disorders
thrombosis - abnormal clotting in unbroken
vessel
thrombus - clot
most likely to occur in leg veins of inactive people
18-68
18-69