Chapter 17 - Blood

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CHAPTER
17
‐
BLOOD
1
Chapter
17
‐
Blood
Overview
of
Blood
Circulation
•
•
•
•
•
•
Blood
leaves
the
heart
via
arteries
that
branch
repeatedly
until
they
become
capillaries
Oxygen
(O2)
and
nutrients
diffuse
across
capillary
walls
and
enter
tissues
Carbon
dioxide
(CO2)
and
wastes
move
from
tissues
into
the
blood
Oxygen‐deficient
blood
leaves
the
capillaries
and
flows
in
veins
to
the
heart
This
blood
flows
to
the
lungs
where
it
releases
CO2
and
picks
up
O2
The
oxygen‐rich
blood
returns
to
the
heart
Composition
of
Blood
•
•
•
•
Blood
is
the
body’s
only
fluid
tissue
It
is
composed
of
liquid
plasma
and
formed
elements
Formed
elements
include:
• Erythrocytes,
or
red
blood
cells
(RBCs)
• Leukocytes,
or
white
blood
cells
(WBCs)
• Platelets
Hematocrit
–
the
percentage
of
RBCs
out
of
the
total
blood
volume
Physical
Characteristics
and
Volume
•
•
•
•
•
•
Blood
is
a
sticky,
opaque
fluid
with
a
metallic
taste
Color
varies
from
scarlet
(oxygen‐rich)
to
dark
red
(oxygen‐poor)
The
pH
of
blood
is
7.35–7.45
Temperature
is
38°C,
slightly
higher
than
“normal”
body
temperature
Blood
accounts
for
approximately
8%
of
body
weight
Average
volume
of
blood
is
5–6
L
for
males,
and
4–5
L
for
females
Functions
of
Blood
•
Blood
performs
a
number
of
functions
dealing
with:
• Substance
distribution
• Regulation
of
blood
levels
of
particular
substances
• Body
protection
Distribution
•
Blood
transports:
• Oxygen
from
the
lungs
and
nutrients
from
the
digestive
tract
• Metabolic
wastes
from
cells
to
the
lungs
and
kidneys
for
elimination
• Hormones
from
endocrine
glands
to
target
organs
Regulation
•
Blood
maintains:
• Appropriate
body
temperature
by
absorbing
and
distributing
heat
• Normal
pH
in
body
tissues
using
buffer
systems
• Adequate
fluid
volume
in
the
circulatory
system
2
CHAPTER
17
‐
BLOOD
Protection
•
•
Blood
prevents
blood
loss
by:
• Activating
plasma
proteins
and
platelets
• Initiating
clot
formation
when
a
vessel
is
broken
Blood
prevents
infection
by:
• Synthesizing
and
utilizing
antibodies
• Activating
complement
proteins
• Activating
WBCs
to
defend
the
body
against
foreign
invaders
Blood
Plasma
•
Blood
plasma
contains
over
100
solutes,
including:
• Proteins
–
albumin,
globulins,
clotting
proteins,
and
others
• Nonprotein
nitrogenous
substances
–
lactic
acid,
urea,
creatinine
• Organic
nutrients
–
glucose,
carbohydrates,
amino
acids
• Electrolytes
–
sodium,
potassium,
calcium,
chloride,
bicarbonate
• Respiratory
gases
–
oxygen
and
carbon
dioxide
Formed
Elements
•
•
•
Erythrocytes,
leukocytes,
and
platelets
make
up
the
formed
elements
• Only
WBCs
are
complete
cells
• RBCs
have
no
nuclei
or
organelles,
and
platelets
are
just
cell
fragments
Most
formed
elements
survive
in
the
bloodstream
for
only
a
few
days
Most
blood
cells
do
not
divide
but
are
renewed
by
cells
in
bone
marrow
Erythrocytes
(RBCs)
•
•
•
•
•
Biconcave
discs,
anucleate,
essentially
no
organelles
Filled
with
hemoglobin
(Hb),
a
protein
that
functions
in
gas
transport
Contain
the
plasma
membrane
protein
spectrin
that:
Gives
erythrocytes
their
flexibility
• Allows
them
to
change
shape
as
necessary
• Erythrocytes
are
an
example
of
the
complementarity
of
structure
and
function
Structural
characteristics
that
contribute
to
its
gas
transport
function
are:
• Biconcave
shape
that
has
a
huge
surface
area
to
volume
ratio
• Discounting
water
content,
erythrocytes
are
97%
hemoglobin
• ATP
is
generated
anaerobically,
so
the
erythrocytes
do
not
consume
the
oxygen
they
transport
Erythrocyte
Function
•
•
•
•
Erythrocytes
are
dedicated
to
respiratory
gas
transport
Hemoglobin
reversibly
binds
with
oxygen
and
most
oxygen
in
the
blood
is
bound
to
hemoglobin
Hemoglobin
is
composed
of:
• The
protein
globin,
made
up
of
two
alpha
and
two
beta
chains,
each
bound
to
a
heme
group
• Each
heme
group
bears
an
atom
of
iron,
which
can
bind
one
to
oxygen
molecule
Each
hemoglobin
molecule
can
transport
four
molecules
of
oxygen
Hemoglobin
(Hb)
•
•
•
Oxyhemoglobin
–
hemoglobin
bound
to
oxygen
• Oxygen
loading
takes
place
in
the
lungs
Deoxyhemoglobin
–
hemoglobin
after
oxygen
diffuses
into
tissues
(reduced
Hb)
Carbaminohemoglobin
–
hemoglobin
bound
to
carbon
dioxide
• Carbon
dioxide
loading
takes
place
in
the
tissues
CHAPTER
17
‐
BLOOD
3
Production
of
Blood
Cells
•
•
•
Hematopoiesis
–
blood
cell
formation
Hemopoiesis
occurs
in
the
red
bone
marrow
of
the:
• Axial
skeleton
and
girdles
• Epiphyses
of
the
humerus
and
femur
Hemocytoblasts
give
rise
to
all
formed
elements
Production
of
Erythrocytes:
Erythropoiesis
•
•
•
•
•
•
A
hemocytoblast
is
transformed
into
a
committed
cell
called
the
proerythroblast
Proerythroblasts
develop
into
early
erythroblasts
The
developmental
pathway
consists
of
three
phases
• Phase
1
–
ribosome
synthesis
in
early
erythroblasts
• Phase
2
–
hemoglobin
accumulation
in
late
erythroblasts
and
normoblasts
• Phase
3
–
ejection
of
the
nucleus
from
normoblasts
and
formation
of
reticulocytes
Reticulocytes
then
become
mature
erythrocytes
Circulating
erythrocytes
–
the
number
remains
constant
and
reflects
a
balance
between
RBC
production
and
destruction
• Too
few
red
blood
cells
leads
to
tissue
hypoxia
• Too
many
red
blood
cells
causes
undesirable
blood
viscosity
Erythropoiesis
is
hormonally
controlled
and
depends
on
adequate
supplies
of
iron,
amino
acids,
and
B
vitamins
Hormonal
Control
of
Erythropoiesis
•
•
Erythropoietin
(EPO)
release
by
the
kidneys
is
triggered
by:
• Hypoxia
due
to
decreased
RBCs
• Decreased
oxygen
availability
• Increased
tissue
demand
for
oxygen
Enhanced
erythropoiesis
increases
the:
• RBC
count
in
circulating
blood
• Oxygen
carrying
ability
of
the
blood
increases
Erythropoiesis:
Nutrient
Requirements
•
•
•
•
Erythropoiesis
requires:
• Proteins,
lipids,
and
carbohydrates
• Iron,
vitamin
B12,
and
folic
acid
The
body
stores
iron
in
Hb
(65%),
the
liver,
spleen,
and
bone
marrow
Intracellular
iron
is
stored
in
protein‐iron
complexes
such
as
ferritin
and
hemosiderin
Circulating
iron
is
loosely
bound
to
the
transport
protein
transferrin
Fate
and
Destruction
of
Erythrocytes
•
•
•
•
The
life
span
of
an
erythrocyte
is
100–120
days
Old
erythrocytes
become
rigid
and
fragile,
and
their
hemoglobin
begins
to
degenerate
Dying
erythrocytes
are
engulfed
by
macrophages
Heme
and
globin
are
separated
and
the
iron
is
salvaged
for
reuse
Fate
of
Hemoglobin
•
•
•
•
•
Heme
is
degraded
to
a
yellow
pigment
called
bilirubin
The
liver
secretes
bilirubin
into
the
intestines
as
bile
The
intestines
metabolize
it
into
urobilinogen
This
degraded
pigment
leaves
the
body
in
feces,
in
a
pigment
called
stercobilin
Globin
is
metabolized
into
amino
acids
and
is
released
into
the
circulation
4
CHAPTER
17
‐
BLOOD
Life
Cycle
of
Red
Blood
Cells
Erythrocyte
Disorders
• Anemia
–
blood
has
abnormally
low
oxygen‐carrying
capacity
• It
is
a
symptom
rather
than
a
disease
itself
• Blood
oxygen
levels
cannot
support
normal
metabolism
• Signs/symptoms
include
fatigue,
paleness,
shortness
of
breath,
and
chills
Anemia:
Insufficient
Erythrocytes
•
•
•
Hemorrhagic
anemia
–
result
of
acute
or
chronic
loss
of
blood
Hemolytic
anemia
–
prematurely
ruptured
erythrocytes
Aplastic
anemia
–
destruction
or
inhibition
of
red
bone
marrow
Anemia:
Decreased
Hemoglobin
Content
•
•
Iron‐deficiency
anemia
results
from:
• A
secondary
result
of
hemorrhagic
anemia
• Inadequate
intake
of
iron‐containing
foods
• Impaired
iron
absorption
Pernicious
anemia
results
from:
• Deficiency
of
vitamin
B12
• Often
caused
by
lack
of
intrinsic
factor
needed
for
absorption
of
B12
Anemia:
Abnormal
Hemoglobin
•
•
Thalassemias
–
absent
or
faulty
globin
chain
in
hemoglobin
• Erythrocytes
are
thin,
delicate,
and
deficient
in
hemoglobin
Sickle‐cell
anemia
–
results
from
a
defective
gene
coding
for
an
abnormal
hemoglobin
called
hemoglobin S (HbS)
• HbS
has
a
single
amino
acid
substitution
in
the
beta
chain
• This
defect
causes
RBCs
to
become
sickle‐shaped
in
low
oxygen
situations
Polycythemia
•
•
Polycythemia
–
excess
RBCs
that
increase
blood
viscosity
Three
main
polycythemias
are:
• Polycythemia
vera
• Secondary
polycythemia
• Blood
doping
Leukocytes
(WBCs)
•
•
Leukocytes,
the
only
blood
components
that
are
complete
cells:
• Are
less
numerous
than
RBCs
• Make
up
1%
of
the
total
blood
volume
• Can
leave
capillaries
via
diapedesis
• Move
through
tissue
spaces
Leukocytosis
–
WBC
count
over
11,000
per
cubic
millimeter
• Normal
response
to
bacterial
or
viral
invasion
Classification
of
Leukocytes:
Granulocytes
•
Granulocytes
–
neutrophils,
eosinophils,
and
basophils
• Contain
cytoplasmic
granules
that
stain
specifically
(acidic,
basic,
or
both)
with
Wright’s
stain
• Are
larger
and
usually
shorter‐lived
than
RBCs
• Have
lobed
nuclei
• Are
all
phagocytic
cells
CHAPTER
17
‐
BLOOD
5
Neutrophils
•
•
Neutrophils
have
two
types
of
granules
that:
• Take
up
both
acidic
and
basic
dyes
• Give
the
cytoplasm
a
lilac
color
• Contain
peroxidases,
hydrolytic
enzymes,
and
defensins
(antibiotic‐like
proteins)
Neutrophils
are
our
body’s
bacterial
slayers
Eosinophils
•
Eosinophils
account
for
1–4%
of
WBCs
• Have
red‐staining,
bi‐lobed
nuclei
connected
via
a
broad
band
of
nuclear
material
• Have
red
to
crimson
(acidophilic)
large,
coarse,
lysosome‐like
granules
• Lead
the
body’s
counterattack
against
parasitic
worms
• Lessen
the
severity
of
allergies
by
phagocytizing
immune
complexes
Basophils
•
Account
for
0.5%
of
WBCs
and:
• Have
U‐
or
S‐shaped
nuclei
with
two
or
three
conspicuous
constrictions
• Are
functionally
similar
to
mast
cells
• Have
large,
purplish‐black
(basophilic)
granules
that
contain
histamine
• Histamine
–
inflammatory
chemical
that
acts
as
a
vasodilator
and
attracts
other
WBCs
Agranulocytes
•
Agranulocytes
–
lymphocytes
and
monocytes:
• Lack
visible
cytoplasmic
granules
• Are
similar
structurally,
but
are
functionally
distinct
and
unrelated
cell
types
• Have
spherical
(lymphocytes)
or
kidney‐shaped
(monocytes)
nuclei
Lymphocytes
•
•
•
Have
large,
dark‐purple,
circular
nuclei
with
a
thin
rim
of
blue
cytoplasm
Found
mostly
enmeshed
in
lymphoid
tissue
(some
circulate
in
the
blood)
There
are
two
types
of
lymphocytes:
T
cells
and
B
cells
• T
cells
function
in
the
immune
response
• B
cells
give
rise
to
plasma
cells,
which
produce
antibodies
Monocytes
•
•
Monocytes
account
for
4–8%
of
leukocytes
• They
are
the
largest
leukocytes
• They
have
abundant
pale‐blue
cytoplasms
• They
have
purple
staining,
U‐
or
kidney‐shaped
nuclei
• They
leave
the
circulation,
enter
tissue,
and
differentiate
into
macrophages
Macrophages:
• Are
highly
mobile
and
actively
phagocytic
• Activate
lymphocytes
to
mount
an
immune
response
Production
of
Leukocytes
•
•
•
Leukopoiesis
is
hormonally
stimulated
by
two
families
of
cytokines
(hematopoetic
factors)
–
interleukins
and
colony‐stimulating
factors
(CSFs)
• Interleukins
are
numbered
(e.g.,
IL‐1,
IL‐2),
whereas
CSFs
are
named
for
the
WBCs
they
stimulate
(e.g.,
granulocyte‐CSF
stimulates
granulocytes)
Macrophages
and
T
cells
are
the
most
important
sources
of
cytokines
Many
hematopoietic
hormones
are
used
clinically
to
stimulate
bone
marrow
6
CHAPTER
17
‐
BLOOD
Formation
of
Leukocytes
•
•
•
•
•
•
•
All
leukocytes
originate
from
hemocytoblasts
Hemocytoblasts
differentiate
into
myeloid
stem
cells
and
lymphoid
stem
cells
Myeloid
stem
cells
become
myeloblasts
or
monoblasts
Lymphoid
stem
cells
become
lymphoblasts
Myeloblasts
develop
into
eosinophils,
neutrophils,
and
basophils
Monoblasts
develop
into
monocytes
Lymphoblasts
develop
into
lymphocytes
Leukocyte
Disorders:
Leukemias
•
•
•
•
Leukemia
refer
to
cancerous
conditions
involving
white
blood
cells
Leukemias
are
named
according
to
the
abnormal
white
blood
cells
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
•
•
•
•
•
Immature
white
blood
cells
are
found
in
the
bloodstream
in
all
leukemias
Bone
marrow
becomes
totally
occupied
with
cancerous
leukocytes
The
white
blood
cells
produced,
though
numerous,
are
not
functional
Death
is
caused
by
internal
hemorrhage
and
overwhelming
infections
Treatments
include
irradiation,
antileukemic
drugs,
and
bone
marrow
transplants
Platelets
•
•
•
Platelets
are
fragments
of
megakaryocytes
with
a
blue‐staining
outer
region
and
a
purple
granular
center
The
granules
contain
serotonin,
Ca2+,
enzymes,
ADP,
and
platelet‐derived
growth
factor
(PDGF)
Platelets
function
in
the
clotting
mechanism
by
forming
a
temporary
plug
that
helps
seal
breaks
in
blood
vessels
Genesis
of
Platelets
•
•
The
stem
cell
for
platelets
is
the
hemocytoblast
The
sequential
developmental
pathway
is
hemocytoblast,
megakaryoblast,
promegakaryocyte,
megakaryocyte,
and
platelets
Hemostasis
•
•
A
series
of
reactions
designed
for
stoppage
of
bleeding
During
hemostasis,
three
phases
occur
in
rapid
sequence
• Vascular
spasms
–
immediate
vasoconstriction
in
response
to
injury
• Platelet
plug
formation
• Coagulation
(blood
clotting)
Platelet
Plug
Formation
•
•
•
Platelets
do
not
stick
to
each
other
or
to
the
endothelial
lining
of
blood
vessels
Upon
damage
to
a
blood
vessel,
platelets:
• Are
stimulated
by
thromboxane
A2
• Stick
to
exposed
collagen
fibers
and
form
a
platelet
plug
• Release
serotonin
and
ADP,
which
attract
still
more
platelets
The
platelet
plug
is
limited
to
the
immediate
area
of
injury
by
PGI2
CHAPTER
17
‐
BLOOD
7
Coagulation
•
•
•
A
set
of
reactions
in
which
blood
is
transformed
from
a
liquid
to
a
gel
Coagulation
follows
intrinsic
and
extrinsic
pathways
The
final
thee
steps
of
this
series
of
reactions
are:
• Prothrombin
activator
is
formed
• Prothrombin
is
converted
into
thrombin
• Thrombin
catalyzes
the
joining
of
fibrinogen
into
a
fibrin
mesh
Detailed
Reactions
of
Hemostasis
Coagulation
Phase
1:
Two
Pathways
to
Prothrombin
Activator
• May
be
initiated
by
either
the
intrinsic
or
extrinsic
pathway
• Triggered
by
tissue‐damaging
events
• Involves
a
series
of
procoagulants
• Each
pathway
cascades
toward
factor
X
• Once
factor
X
has
been
activated,
it
complexes
with
calcium
ions,
PF3,
and
factor
V
to
form
prothrombin
activator
Coagulation
Phase
2:
Pathway
to
Thrombin
• Prothrombin
activator
catalyzes
the
transformation
of
prothrombin
to
the
active
the
enzyme
thrombin
Coagulation
Phase
3:
Common
Pathways
to
the
Fibrin
Mesh
• Thrombin
catalyzes
the
polymerization
of
fibrinogen
into
fibrin
• Insoluble
fibrin
strands
form
the
structural
basis
of
a
clot
• Fibrin
causes
plasma
to
become
a
gel‐like
trap
• Fibrin
in
the
presence
of
calcium
ions
activates
factor
XIII
that:
• Cross‐links
fibrin
• Strengthens
and
stabilizes
the
clot
Clot
Retraction
and
Repair
•
•
Clot
retraction
–
stabilization
of
the
clot
by
squeezing
serum
from
the
fibrin
strands
Repair
• Platelet‐derived
growth
factor
(PDGF)
stimulates
rebuilding
of
blood
vessel
wall
• Fibroblasts
form
a
connective
tissue
patch
• Endothelial
cells
multiply
and
restore
the
endothelial
lining
Factors
Limiting
Clot
Growth
or
Formation
•
Two
homeostatic
mechanisms
prevent
clots
from
becoming
large
• Swift
removal
of
clotting
factors
• Inhibition
of
activated
clotting
factors
Inhibition
of
Clotting
Factors
•
•
•
Fibrin
acts
as
an
anticoagulant
by
binding
thrombin
and
preventing
its:
• Positive
feedback
effects
of
coagulation
• Ability
to
speed
up
the
production
of
prothrombin
activator
via
factor
V
• Acceleration
of
the
intrinsic
pathway
by
activating
platelets
Thrombin
not
absorbed
to
fibrin
is
inactivated
by
antithrombin
III
Heparin,
another
anticoagulant,
also
inhibits
thrombin
activity
8
CHAPTER
17
‐
BLOOD
Factors
Preventing
Undesirable
Clotting
•
•
Unnecessary
clotting
is
prevented
by
the
structural
and
molecular
characteristics
of
endothelial
cells
lining
the
blood
vessels
Platelet
adhesion
is
prevented
by:
• The
smooth
endothelial
lining
of
blood
vessels
• Heparin
and
PGI2
secreted
by
endothelial
cells
• Vitamin
E
quinone,
a
potent
anticoagulant
Hemostasis
Disorders:
Thromboembolytic
Disorders
•
•
Thrombus
–
a
clot
that
develops
and
persist
in
an
unbroken
blood
vessel
• Thrombi
can
block
circulation,
resulting
in
tissue
death
• Coronary
thrombosis
–
thrombus
in
blood
vessel
of
the
heart
Embolus
–
a
thrombus
freely
floating
in
the
blood
stream
• Pulmonary
emboli
can
impair
the
ability
of
the
body
to
obtain
oxygen
• Cerebral
emboli
can
cause
strokes
Prevention
of
Undesirable
Clots
•
Substances
used
to
prevent
undesirable
clots
include:
• Aspirin
–
an
antiprostaglandin
that
inhibits
thromboxane
A2
• Heparin
–
an
anticoagulant
used
clinically
for
pre‐
and
postoperative
cardiac
care
• Warfarinin
–
used
for
those
prone
to
atrial
fibrillation
• Flavonoids
–
substances
found
in
tea,
red
wine,
and
grape
juice
that
have
natural
anticoagulant
activity
Hemostasis
Disorders:
Bleeding
Disorders
•
Thrombocytopenia
–
condition
where
the
number
of
circulating
platelets
is
deficient
• Patients
show
petechiae
(small
purple
blotches
on
the
skin)
due
to
spontaneous,
widespread
hemorrhage
• Caused
by
suppression
or
destruction
of
bone
marrow
(e.g.,
malignancy,
radiation)
• Platelet
counts
less
than
50,000/mm3
is
diagnostic
for
this
condition
• Treated
with
whole
blood
transfusions
Hemostasis
Disorders:
Bleeding
Disorders
•
•
•
•
•
•
•
Inability
to
synthesize
procoagulants
by
the
liver
results
in
severe
bleeding
disorders
Causes
can
range
from
vitamin
K
deficiency
to
hepatitis
and
cirrhosis
Inability
to
absorb
fat
can
lead
to
vitamin
K
deficiencies
as
it
is
a
fat‐soluble
substance
and
is
absorbed
along
with
fat
Liver
disease
can
also
prevent
the
liver
from
producing
bile,
which
is
required
for
fat
and
vitamin
K
absorption
Hemophilias
–
hereditary
bleeding
disorders
caused
by
lack
of
clotting
factors
• Hemophilia
A
–
most
common
type
(83%
of
all
cases)
due
to
a
deficiency
of
factor
VIII
• Hemophilia
B
–
results
from
a
deficiency
of
factor
IX
• Hemophilia
C
–
mild
type,
caused
by
a
deficiency
of
factor
XI
Symptoms
include
prolonged
bleeding
and
painful
and
disabled
joints
Treatment
is
with
blood
transfusions
and
the
injection
of
missing
factors
CHAPTER
17
‐
BLOOD
9
Blood
Transfusions
•
•
•
Transfusions
are
necessary:
• When
substantial
blood
loss
occurs
• In
certain
hemostatis
disorders
Whole
blood
transfusions
are
used:
• When
blood
loss
is
substantial
• In
treating
thrombocytopenia
Packed
red
cells
(cells
with
plasma
removed)
are
used
to
treat
anemia
Human
Blood
Groups
•
•
•
•
•
•
RBC
membranes
have
glycoprotein
antigens
on
their
external
surfaces
These
antigens
are:
• Unique
to
the
individual
• Recognized
as
foreign
if
transfused
into
another
individual
• Promoters
of
agglutination
and
are
referred
to
as
agglutinogens
Presence/absence
of
these
antigens
are
used
to
classify
blood
groups
Humans
have
30
varieties
of
naturally
occurring
RBC
antigens
The
antigens
of
the
ABO
and
Rh
blood
groups
cause
vigorous
transfusion
reactions
when
they
are
improperly
transfused
Other
blood
groups
(M,
N,
Dufy,
Kell,
and
Lewis)
are
mainly
used
for
legalities
ABO
Blood
Groups
•
•
•
The
ABO
blood
groups
consists
of:
• Two
antigens
(A
and
B)
on
the
surface
of
the
RBCs
• Two
antibodies
in
the
plasma
(anti‐A
and
anti‐B)
An
individual
with
ABO
blood
may
have
various
types
of
antigens
and
spontaneously
preformed
antibodies
Agglutinogens
and
their
corresponding
antibodies
cannot
be
mixed
without
serious
hemolytic
reactions
Rh
Blood
Groups
•
•
•
•
•
There
are
eight
different
Rh
agglutinogens,
three
of
which
(C,
D,
and
E)
are
common
Presence
of
the
Rh
agglutinogens
on
RBCs
is
indicated
as
Rh+
Anti‐Rh
antibodies
are
not
spontaneously
formed
in
Rh–
individuals
However,
if
an
Rh–
individual
receives
Rh+
blood,
anti‐Rh
antibodies
form
A
second
expose
to
Rh+
blood
will
result
in
a
typical
transfusion
reaction
Hemolytic
Disease
of
the
Newborn
•
•
•
•
Hemolytic
disease
of
the
newborn
–
Rh+
antibodies
of
a
sensitized
Rh–
mother
cross
the
placenta
and
attack
and
destroy
the
RBCs
of
an
Rh+
baby
Rh–
mother
become
sensitized
when
Rh+
blood
(from
a
previous
pregnancy
of
an
Rh+
baby
or
a
Rh+
transfusion)
causes
her
body
to
synthesis
Rh+
antibodies
The
drug
RhoGAM
can
prevent
the
Rh–
mother
from
becoming
sensitized
Treatment
of
hemolytic
disease
of
the
newborn
involves
pre‐birth
transfusions
and
exchange
transfusions
after
birth
10
CHAPTER
17
‐
BLOOD
Transfusion
Reactions
•
•
•
Transfusion
reactions
occur
when
mismatched
blood
is
infused
Donor’s
cells
are
attacked
by
the
recipient’s
plasma
agglutinins
causing:
• Diminished
oxygen‐carrying
capacity
• Clumped
cells
that
impede
blood
flow
• Ruptured
RBCs
that
release
free
hemoglobin
into
the
bloodstream
Circulating
hemoglobin
precipitates
in
the
kidneys
and
causes
renal
failure
Blood
Typing
•
•
When
serum
containing
anti‐A
or
anti‐B
agglutinins
is
added
to
blood,
agglutination
will
occur
between
the
agglutinin
and
the
corresponding
agglutinogens
Positive
reactions
indicate
agglutination
Plasma
Volume
Expanders
•
•
•
•
When
shock
is
imminent
from
low
blood
volume,
volume
must
be
replaced
Plasma
or
plasma
expanders
can
be
administered
Plasma
expanders:
• Have
osmotic
properties
that
directly
increase
fluid
volume
• Are
used
when
plasma
is
not
available
• Examples:
purified
human
serum
albumin,
plasminate
and
dextran
Isotonic
saline
can
also
be
used
to
replace
lost
blood
volume
Diagnostic
Blood
Tests
•
•
•
Laboratory
examination
of
blood
can
assess
an
individual’s
state
of
health
Microscopic
examination:
• Variations
in
size
and
shape
of
RBCs
–
predictions
of
anemias
• Type
and
number
of
WBCs
–
diagnostic
of
various
diseases
Chemical
analysis
can
provide
a
comprehensive
picture
of
one’s
general
health
status
in
relation
to
normal
values
Developmental
Aspects
•
•
•
•
Before
birth,
blood
cell
formation
takes
place
in
the
fetal
yolk
sac,
liver,
and
spleen
By
the
7th
month,
red
bone
marrow
is
the
primary
hematopoietic
area
Blood
cells
develop
from
mesenchymal
cells
called
blood islands
The
fetus
forms
HbF,
which
has
a
higher
affinity
for
oxygen
than
adult
hemoglobin
Developmental
Aspects
•
•
•
Age‐related
blood
problems
result
from
disorders
of
the
heart,
blood
vessels,
and
the
immune
system
Increased
leukemias
are
thought
to
be
due
to
the
waning
deficiency
of
the
immune
system
Abnormal
thrombus
and
embolus
formation
reflects
the
progress
of
atherosclerosis

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