Multipotent uncommitted stem cell
IL-1, IL-6,IL-3
Hematology
Committed myeloid stem cell
Committed lymphoid stem cell
Erythropoiesis
hemocytoblast,
todiscs,
committed
cell:
Functions
Erythrocytes
of
Blood
(RBCs)
Substance
Biconcave
distribution
anucleate,
(Blood
Erythrocyte
Disorders
anemia
Bd
has
abnormally
Erythropoiesis:
Nutrient
Requirements
proerythroblast,
to early
erythroblasts
in hormones
3 phases:
transport
essentially
O
no
,
nutrients,
organelles,
metabolic
filled
with
waste,
hemoglobin
Fate
and
Destruction
of
Erythrocytes
life
span
of
2
low
O
-carrying
capacity,
it
is
a
symptom
rather
Blood
Anemia:
Decreased
contains
Hemoglobin
over
100
solutes,
Content
including:
iron2Plasma
Erythropoiesis
requires:
Phase
1
ribosome
synthesis
in
early
erythroblasts,
Physical
Classification
Characteristics
of
Leukocytes:
and
Volume
Formed
Leukocytes
Elements:
(WBCs)
RBC,
complete
WBC
cells:
&
platelets:
less
numerous
Only
),
(Hb):
Regulation
protein
of
that
Bd
functions
levels
of
particular
in
gas
transport,
substances
RBC
is
100–120
days,
old
RBC
rigid
and
fragile,
Erythrocyte
Anemia:
Abnormal
Function
Hemoglobin
respiratory
thalassemias
gas
transport:
Hormonal
Control
of
Erythropoiesis
erythropoietin
than
a 2disease
itself,
Bd
Ofrom:
levels
cannot
support
Proteins
deficiency
(albumin,
anemia
results
globulins,
clotting
secondary
proteins,
result
...),
of
2
Hemoglobin
Polycythemia
(Hb)
excess
oxyhemoglobin
RBCs
increase
Hb
Bd
bound
viscosity,
to
O
,
Proteins,
lipids,
and
carbohydrates,
iron,
vitamin
Composition
Production
of
of
Blood
Blood:
Cells
the
hematopoiesis
body’s
only
fluid
Bd
tissue,
cell
Phase
Hb
accumulation
in
late
erythroblasts
&
2
Blood
Granulocytes
is
a
sticky,
neutrophils,
opaque
fluid
eosinophils,
with
a
metallic
&
basophils,
taste
WBCs
than
RBCs,
are
complete
make
up
cells,
1%
of
RBCs
the
total
have
blood
no
nuclei
volume
or
(maintains
contain
PM
appropriate
protein
spectrin
temp.
that:
by
absorbing
gives
RBC
&their
their
Hb
degenerate,
engulfed
byHb,
macrophages,
Hb
absent
reversibly
or
faulty
binds
globin
with
chain
O
,
Hb
in
is
composed
RBC
thin,
of:
(EPO)
release
by
kidneys
is
triggered
by:
Hypoxia
2
normal
metabolism,
signs/symptoms:
fatigue,
nonprotein
hemorrhagic
nitrogenous
anemia,
inadequate
substances
intake
(lactic
of
acid,
iron3O
main
loading
polycythemias
takes
place
are:
in
lungs,
deoxyhemoglobin
B12,
and
folic
acid
composed
formation,
of
occurs
liquid
in
plasma
red
bone
&
formed
marrow
elements,
of
axial
normoblasts,
Phase
3
ejection
of
nucleus
from
nor2
color
contain
varies
cytoplasmic
from
scarlet
granules
(oxygen-rich)
that
stain
to
specifically
dark
red
organelles,
can
leave
capillaries
platelets
are
via
just
diapedesis,
cell
fragments,
move
through
most
distributing
flexibility,
allows
heat,
to
normal
change
pH
shape
in
body
as
necessary,
tissues:
buffer
heme
&
globin
separated,
iron
is
salvaged
for
reuse
protein
delicate,
globin:
and
deficient
2
alpha
in
&
Hb,
2
beta
sickle-cell
chains,
anemia
each
bound
due
to
decreased
RBCs,
decreased
O
availability,
paleness,
shortness
of
breath
&
chills
2
urea,
containing
creatinine),
foods,
organic
impaired
nutrients
iron
absorption,
(glucose,
carboHb
Polycythemia
after
O
diffuses
vera
into
tissues
(reduced
Hb),
The
body
stores
iron
in
Hb
(65%),
the
liver,
spleen,
formed
skeleton
include:
&
girdles,
erythrocytes
epiphyses
of
or
humerus
red
blood
&
cells
femur,
moblasts:
formation
of
reticulocytes,
then
mature
2
(oxygen-poor),
(acidic,
basic,
or
pH
both)
of
blood
with
is
Wright’s
7.35–7.45,
stain,
temp.
larger
is of
formed
tissue
spaces,
elements
leukocytosis
survive
in
WBC
bloodstream
count
over
for
11,000
only
systems,
RBC
are
adequate
example
of
fluid
complementarity
volume),
Body
of
protection
structure
Fate
of
Hemoglobin
heme
degraded
to
a
yellow
to
results
a
heme
from
group,
defective
each
gene
heme
coding
group
for
bears
an
an
abnormal
atom
increased
tissue
demand
for
O2 ,iron
enhanced
Anemia:
Insufficient
Erythrocytes
hemorrhagic
hydrates,
pernicious
amino
anemia
acids),
results
electrolytes
from:
deficiency
(sodium,
of in
Carbaminohemoglobin
Secondary
polycythemia
Hb
bound
to
CO
,
CO
and
bone
marrow,
intracellular
is
stored
(RBCs),
hemocytoblasts
leukocytes
give
or
rise
white
to
all
blood
formed
cells
elements
(WBCs)
erythrocytes.
Circulating
RBC
number
remains
2
2 &
38°C,
and
usually
slightly
shorter-lived
higher
than
than
“normal”
RBCs,
body
have
temp.
lobed
few
per
cubic
days,
most
millimeter,
blood
normal
cells
do
response
not
divide
to
but
bacterial
are
(prevents
&
function:
blood
biconcave
loss:
activating
shape
has
plasma
huge
surface
proteins
area
&
pigment
bilirubin,
liver
secretes
bilirubin
as
bile
to
iron,
Hb
called
which
HbS:
can
has
bind
single
one
to
aa
O
substitution
molecule,
each
in
beta
Hb
erythropoiesis
increases:
RBC
count
in
circulating
2
anemia
result
of
acute
or
chronic
loss
of
Bd,
potassium,
vitamin
B12,
calcium,
often
caused
chloride,
by
lack
bicarbonate),
of
intrinsic
respirafactor
loading
Blood
doping
takes
place
in
tissues
protein-iron
complexes
as
ferritin
&
hemosiderin,
platelets.
Hematocrit
is
%
of
RBCs
of
total
Bd
vol.
constant:
balance
of
production
&
destruction.
it
nuclei,
is
8%
all
of
phagocytic
body
weight,
cells
average
vol.
of
Bd
is
5–6
L
renewed
or
viral
invasion
by
cells
in
bone
marrow
platelets,
to
vol.
ratio,
clot
discounting
formation,
water
blood
prevents
content,
RBC
infection:
are
intestines,
metabolized
into
urobilinogen,
leaves
molecule
chain,
causes
can
transport
RBCs
to
become
4
molecules
sickle-shaped
of
O
in
low
blood,
Ofor
ability
of thedioxide)
blood
increases
2 RBC
hemolytic
anemia
prematurely
ruptured
2 carrying
tory
needed
gases
(oxygen
absorption
and
of
carbon
B12
circulating
iron
is
loosely
bound
to
the
transport
Too
few
RBC:
tissue
hypoxia,
too
many
RBC:
for
males,
and
4–5
L
for
females
synthesizing
97%
Hb,
ATP
&
is
utilizing
generated
antibodies,
anaerobically,
activating
so
RBC
combody
in situations
feces:
pigment
calledor
stercobilin,
globin
is
oxygen
Aplastic
anemia
destruction
inhibition
of
red
protein
transferrin
undesirable
viscosity.
Erythropoiesis
is hormonally
plement
do
not
consume
proteins,
O
activating
WBC
against
invader)
metabolized
into
aa
&
released
into
circulation
2
bone
marrow
controlled, depends supplies of iron, aa, B vitamins
CSF-GM
CFU-Meg
CFU-E
CFU-GM
Erythropoietin
CSF-G
CSF-M
Myeloblast
Megakaryoblast
Lymphoblast
Proerythroblast
Promyelocyte
Monoblast
Early normpblast
Megakaryocyte
Prolymphocyte
E, N, B, Myelocyte
Intermediate normoblast
Promonocyte
E, N, B, Metamyelocyte
Late normoblast
Reticulocyte
Reticulocyte
Granulocyte E, N, B
Monocyte
Platelets
Lymphocyte
Blood
Erythrocyte
Exit
Tissue
BASIM ZWAIN Tissue
LECTURE
Macrophage NOTES
Home
Pathway
Cell
Description
Hematology
Cell Type
Type Intrinsic
Description
DD and
LS
Function
Cells/L
and
LS
Function
Cells/L
Intrinsic
Pathway
Extrinsic
Pathway
System for
naming blood
– clotting
factors
Extrinsic
Biconcave
4
–
6
million
D:
5 –pathway
7 days catalyzes
O2 and CO2
Erythrocytes
Inhibition
of
Clotting
Factors
Contact
Tissue thromboplastin(TPL)
Contact
Agranulocytes
Coagulation
Phase
2:
Prothr.
activator
Population
S.
U.
of
%
Groups,
of Blood
Factors
Names
Neutrophils
2Frequency
types
of
granules,
take
up
both
acidic
Human
Blood
Groups
III
Anucleate
disc
LS:
100
–
120
transport
Rh
Blood
Groups
ABO
Blood
Groups D:Disorders
Detailed
Reactions
of
Hemostasis
HMW-K
Tissue
plasminogen
Urokinase
Hemostasis
Disorders:
Bleeding
Fibrinogen
I
•Platelets
Fibrin
acts
as
an
anticoagulant
by
binding
Lymphocytes
Spherical
nucleus
1500
–
3000
days
– weeks
Cellular
or
Production
Prevention
of
of
Undesirable
Leukocytes
Clots
Kallikrein
transformation
of
prothr.
to
active
enz.
thrombin
Hemolytic
Transfusion
Lymphocytes
Disease
Reactions
have
of
large,
the
Newborn
dark-purple,
circular
days
&
basic
dyes,
cytoplasm
lilac
colour,
peroxidases,
7-8
m
Leukemia
Platelet
Diagnostic
Plug
Blood
Formation
Tests
activator
(t-PA)
•Plasma
RBC
membranes
have
glycoprotein
antigens
on
Clot
Hemostasis
Hemophilias:
Retraction
Volume
Disorders:
hereditary
Expanders
and
Repair
Bleeding
bleeding
Disorders
disorders
There
are
eight
different
Rh
agglutinogens,
three
Developmental
Aspects
Prothrombin
II
XII
XIIa
Coagulation
Phase
1:
Two
Pathways
to
Factors
Hemostasis
Preventing
Disorders:
Undesirable
Thromboembolytic
Clotting
Pale
blue
LS:
hoursmismatched
–mother
years
antibody
directed
•thrombin
Thrombocytopenia:
condition
where
the
number
Blood
ABO
Blood
Transfusions
Groups
and
preventing
its:
Asian
Black
White
Group
Blood
Leukopoiesis
Fragments
Substances
of
used
is
megakaryocytes
hormonally
to
prevent
undesirable
stimulated
with
a
blueby
clots:
two
Leukocytes
Formation
of
Leukocytes
Phase
3:
Fibrin
Mesh
•Coagulation
nuclei
Transfusion
Rh+
antibodies
with
a
thin
reactions
of
rim
a
sensitized
of
occur
blue
cytoplasm,
when
Rh–
found
cross
HMW-K
hydrolytic
enz.s
&
defensins
(antibiotic-like
prns),
Tissue
thromboplastin
Immature
Platelets
Laboratory
not
white
examination
stick
blood
to
each
cells
of
other
blood
are
found
or
can
to
endothelial
assess
in
the
an
III
Blood
Group
RBC
Antigen
Plasma
Antibody
Blood
that
can
be
received
external
surfaces,
these
antigens
are:
unique
caused
•their
When
Clot
Inability
retraction
by
shock
lack
to
synthesize
is
of
imminent
–
clotting
stabilization
procoagulants
factors
from
of
low
the
blood
clot
by
the
by
volume,
liver
Leukocyte
Hemostasis
Disorders:
Leukemias
XII
XIIa
of
which
(C,
D,
and
E)
are
common
Before
birth,
blood
cell
formation
takes
place
in
cytoplasm
immune
response
Activator
•Prothrombin
Thrombus:
Unnecessary
a
clotting
clot
that
is
develops
prevented
and
by
persist
the
in
an
Granulocytes
Coagulation
of
circulating
platelets
deficient
Transfusions
The
ABO
blood
are
groups
necessary:
consists
of:
Developmental
Aspects
•Blood
Positive
feedback
effects
of
coagulation
Calcium
IV
families
staining
Aspirin:
of
outer
an
cytokines
antiprostaglandin
region
(hematopoetic
and
a
purple
that
granular
factors)
inhibits
–
center
All
leukocytes
originate
from
hemocytoblasts
Typing
Thrombin
catalyzes
polymerization
of
fibrinogen
placenta,
blood
mostly
is
enmeshed
infused
attack
&
in
destroy
lymphoid
RBCs
tissue
of
an
(some
Rh+
in
baby
Bd),
XI
XIa lymphocytes
VIIa
VII
Agranulocytes
and
monocytes:
bacterial
slayers.
Eosinophils
1–4%
of
WBCs,
redbloodstream
lining
individual’s
of
Bd
state
vessels.
in
all
of
leukemias
health
Upon
damage
to
vessel;
they:
to
individual,
recognized
foreign
if
transfused
to
squeezing
•results
volume
Hemophilia
in
must
severe
serum
be
A:
replaced
bleeding
most
from
common
the
disorders
fibrin
type
strands
(83%
of
all
Cancerous
Series
of
reactions
conditions
designed
involving
to
stop
white
bleeding
blood
cells
Neutrophil
Multi-lobed
3000
–
7000
D:
6
–
9
days
Bacterial
Factors
Limiting
Clot
Growth
or
Formation
Presence
of
the
Rh
agglutinogens
on
RBCs
is
5
–
17
m
the
fetal
yolk
sac,
liver,
and
spleen
Proaccelerin
V final
•unbroken
May
be
initiated
by
either
the
intrinsic
or
structural
blood
and
molecular
vessel
characteristics
of
2+of
The
thee
steps
of
this
series
reactions
are:
5
4
4
AB
Ca
Ca
Patients
show
petechiae
(small
purple
blotches
on
When
Two
antigens
substantial
(A
and
blood
B)
on
loss
surface
occurs
of
the
RBCs
•thromboxane
Age-related
blood
problems
result
from
disorders
Ability
to
speed
up
the
production
of
prothrombin
interleukins
Granules
contain
and
A2
colony-stimulating
serotonin,
Ca
,
enzymes,
factors
(CSFs)
ADP,
Hemocytoblasts
to
myeloid
stem
cells
and
Serum
containing
anti-A
or
anti-B
agglutinins
is
AB
A
and
B
None
A,
B,
AB,
and
O
into
fibrin
•another,
two
Rh–
Donor’s
types:
mother
cells
T
cells
become
are
(function
attacked
sensitized:
in
by
immune
the
Rh+
recipient’s
blood
response)
(from
&
nucleus
LS:
6
hours
2
phagocytosis
Lack
visible
cytoplasmic
granules,
similar
TPL
staining,
bi-lobed
nuclei
connected
via
band
of
Are
Bone
Microscopic
stimulated
marrow
examination:
becomes
by
thromboxane
totally
occupied
A2
with
Proconvertin
VII
promoters
of
agglutination:
agglutinogens
Repair
Causes
Plasma
due
can
or
to
plasma
range
a
deficiency
from
expanders
vitamin
of
factor
can
K
VIII
administered:
deficiency
to
Monocytes
Kidney
shaped
100
–
700
D:
2
–
3
days
Phagocytosis
According
Three
phases
to
abnormal
occur
in
rapid
white
sequence
blood
cells
involved:
•cases)
Two
homeostatic
mechanisms
prevent
clots
from
Prekallikrein
activcators
indicated
Rh+
IX as month,
IXa red bone marrow is the
By
the
7th
extrinsic
pathway
•endothelial
Can
block
cells
circulation,
lining
the
resulting
blood
vessels
in
tissue
death
Prothrombin
activator
is
formed
the
skin)
due
to
spontaneous,
widespread
Two
In
certain
antibodies
hemostatis
in
the
disorders
plasma
(anti-A
and
anti-B)
days
of
the
heart,
blood
vessels,
and
the
immune
system
10
–
14
m
via
factor
V
and
•activator
Interleukins
Heparin:
platelet-derived
an
anticoagulant
are
numbered
growth
factor
used
(e.g.,
clinically
IL-1,
(PDGF)
IL-2),
for
CSFs
preAntihemophilic
factor
VIII
lymphoid
stem
cells
added
to
blood,
agglutination
will
occur
between
Insoluble
fibrin
strands
form
the
structural
basis
previous
plasma
B
cells(give
agglutinins
pregnancy
rise
to
plasma
causing:
of
Rh+
cell:
baby
produce
or
transfusion)
antibodies)
structurally,
but
functionally
distinct
&
unrelated
nuclear
material,
has
red
to
crimson(acidophilic)
PL
Ca
•cancerous
Variations
Stick
to
exposed
leukocytes
in
size
collagen
and
shape
fi,
form
of
RBCs
a
platelet
–
plug
nucleus
LS:
months
Develop
into
Presence/absence
of
these
antigens
are
used
to
hepatitis
Platelet-derived
Hemophilia
Plasma
and
expanders
cirrhosis
B:
results
growth
have
of
osmotic
factor
deficiency
(PDGF)
properties
of
factor
stimulates
that
IX
•becoming
Vascular
Myelocytic
spasms
leukemia
(immediate
(involves
vasoconstriction
myeloblasts)
in
large
Anti-Rh
antibodies
are
not
spontaneously
formed
VIII
VIIIa
27
20
11
B
primary
hematopoietic
area
Eosinophil
Bi-lobed
nucleus
100
–
400
D:
6
9
days
Kill
parasitic
Christmas
factor
Triggered
by
tissue-damaging
events
IX B blood
•hemorrhage
Platelet
Coronary
adhesion
thrombosis:
is
prevented
in
Bd
vessel
by:
of
heart
Prothrombin
is
converted
into
thrombin
B
Anti-A
B
and
O
Whole
Individual
with
transfusions
ABO
Bd
may
are
used:
have
various
types
Increased
leukemias
are
thought
to
be
due
to
the
Acceleration
of
the
intrinsic
pathway
by
•are
and
Platelets
named
postoperative
function
for
the
WBCs
cardiac
in
clotting
they
care
mechanism,
stimulate
(e.g.,
forming
Myeloid
stem
cells
to
myeloblasts
or
monoblasts
agglutinin
and
corresponding
agglutinogens
of
a
clot
Gray-blue
macrophages
causes
Monocytes
Diminished
her
body
4–8%
oxygen-carrying
to
of
synthesis
leukocytes,
Rh+
capacity
largest
antibodies
leukocytes,
cell
types,
have
spherical
(lymphocytes)
or
kidneylarge,
coarse,
lysosome-like
granules,
counterattack
•classify
predictions
White
Release
blood
serotonin
of
cells
anemias
produced,
&
ADP
to
attract
though
more
numerous,
platelets
X
Xa
Stuart
– Prower
factor
Red
cytoplasmic
LS:to
8 lymphocytes)
–by
12
days
worms
X removal
groups
rebuilding
directly
Inability
Hemophilia
increase
to
of
absorb
blood
C:
mild
fluid
vessel
fat
type,
volume,
can
wall
caused
lead
used
vitamin
when
a
deficiency
plasma
K
is
•in
response
Lymphocytic
to
injury)
leukemia
(involves
Swift
of
clotting
factors
Rh–
individuals
Blood
cells
develop
from
mesenchymal
cells
called
•waning
Involves
a
series
of
procoagulants
Prekallikrein
Kallikrein
The
Embolus:
smooth
a
thrombus
endothelial
freely
lining
floating
of
blood
in
vessels
Bd
stream
Thrombin
catalyzes
the
joining
of
fibrinogen
into
Caused
by
suppression
or
destruction
of
bone
•activating
of
When
antigens
blood
&
spontaneously
loss
is
substantial
preformed
antibodies
deficiency
of
the
immune
system
platelets
cytoplasm
Common
Pathway
granulocyte-CSF
temporary
Warfarin:
plug,
used
helps
for
stimulates
those
seal
prone
breaks
granulocytes)
to
in
atrial
blood
vessels
Lymphoid
stem
cells
become
lymphoblasts
Plasma
thromboplastin
antecedent
••are
Positive
reactions
indicate
agglutination
XI
Ca
Thrombin
granules
Destroy
antigenFibrin
causes
plasma
to
become
a
gel-like
trap
has
The
Clumped
abundant
drug
cells
RhoGAM
pale-blue
that
impede
can
cytoplasms,
prevent
blood
the
flow
purple
Rh–
mother
staining
shaped
(monocytes)
nuclei
against
parasitic
worm,
lessen
allergies,
phagocyto
Type
Plug
not
is
and
functional
limited
number
to
area
of
WBCs
of
injury
(diagnostic
by
PGI2
of
various
28
27
40
A
Humans
have
30
varieties
of
RBC
antigens
deficiencies
of
not
Fibroblasts
factor
available,
XI
as
form
as
it
purified
is
a
connective
fat-soluble
human
tissue
substance
serum
patch
albumin,
and
is
Acute
Platelet
leukemia
plug
formation
(involves
blast-type
cells
PL factors
Va
V blood,
of
activated
clotting
•Inhibition
However,
if
an
Rh–
individual
receives
Rh+
blood
islands
A
A
Anti-B
A
and
O
Each
pathway
cascades
toward
factor
X
•amarrow
Heparin
Pulmonary
and
emboli
PGI2
can
secreted
impair
by
the
endothelial
ability
of
cells
the
Hageman
factor
XII
fibrin
mesh
antibody
complexby
10
– malignancy,
14
m
(e.g.,
radiation)
Agglutinogens
In
treating
thrombocytopenia
and
their
corresponding
antibodies
14
24
•fibrillation
Abnormal
thrombus
and
embolus
formation
Thrombin
not
absorbed
to
fibrin
is
inactivated
Genesis
Macrophages
of
Platelets
and
T
cells
are
the
most
important
Myeloblasts
to
eosinophils,
neutrophils,
basophils
Fibrin
in
the
presence
of
calcium
ions
activates
•from
U-or
Ruptured
kidney-shaped
becoming
RBCs
sensitized
that
nuclei,
release
leave
free
circulation,
hemoglobin
enter
into
-se
immune
complexes.
Basophils
0.5%
of
WBCs,
Thrombin
Prothrombin
Coagulation
diseases)
Death
is
caused
(a
set
by
of
internal
reactions,
hemorrhage
Bd
transformed
and
•absorbed
Antigens
of
ABO
&
Rh
Bd
groups
cause
vigorous
Fibrin
–
stabilizing
factor
XIII
plasminate
Endothelial
Symptoms
along
and
include
cells
dextran
with
multiply
prolonged
fat
and
bleeding
restore
the
and
painful
Plasmin
Plasminogen
primarily
Coagulation
affects
(blood
children)
clotting)
antibodies
form
Basophilto
Lobed
nucleus
20 –potent
50 activated,
D: 3 –a7 days
Mediates
•anti-Rh
The
fetus
forms
HbF,
which
has
higher
affinity
Once
factor
X
has
been
it
complexes
body
Vitamin
obtain
E
quinone,
oxygen
a
anticoagulant
Platelet
counts
less
than
50,000/mm3
is
diagnostic
•antithrombin
cannot
Packed
mixed
red
cells
without
(cells
serious
with
plasma
hemolytic
removed)
reactions
are
reflects
the
progress
of
atherosclerosis
III
sources
The
Flavonoids:
stem
of
cytokines
cell
substances
for
platelets
found
is
the
in
hemocytoblast
tea,
red
wine,
&
Monoblasts
to
monocytes
Fibrin
Fibrinogen
High
molecular
weight
kininogen
(Fitzgerald
factor)
HMW-K
factor
XIII
that:
•from
the
tissue,
Treatment
bloodstream
differentiate
of
hemolytic
into
macrophages
disease
of
the
newborn
40
49
45
O
U-orS-shaped
nuclei
with
2-3
constrictions,
large
Blue-purple
LS:
hours
–
days
inflammation
overwhelming
Chemical
liquid
analysis
to
gel,
infections
intrinsic
can
provide
&
extrinsic
a
comprehensive
pathways
O disease
None
Anti-A
and
Anti-B
O
transfusion
reactions
when
improperly
transfused
endothelial
•and
Liver
Isotonic
disabled
saline
lining
joints
can
can
also
also
prevent
be
used
the
to
replace
liver
from
lost
Chronic
leukemia
more
prevalent
in
older
people
A
second
expose
to
Rh+
blood
will
result
in
a
for
oxygen
than
adult
hemoglobin
Cytoplasmic
250,000
–
500,000
D:
4
–
5
days
Blood
clotting
Platelets
calcium
ions,
PF3,
and
factor
V
to
form
•with
Cerebral
emboli
can
cause
strokes
Prekallikrein
(Fletcher
factor)
Pre-K
for
this
condition
used
to
treat
anemia
Ca
XIIIa
XIII
••involves
Heparin,
another
anticoagulant,
also
inhibits
cytoplasmic
Heparin
grape
Many
Pathway
juice
hematopoietic
is
that
hemocytoblast,
have
natural
hormones
megakaryoblast,
anticoagulant
are
used
clinically
activity
Lymphoblasts
to
lymphocytes
Cross-links
fibrin
Macrophages
Circulating
pre-birth
hemoglobin
highly
transfusions
mobile
precipitates
&
actively
and
exchange
in
phagocytic,
the
purplish-black
(basophilic)
granules:
histamine
picture
Treatments
of
one’s
include
general
irradiation,
health
status
antileukemic
in
relation
to
•producing
Other
Bd
gps
(M,
N,
Dufy,
Kell,
and
Lewis)
are
blood
Treatment
volume
bile,
is
with
which
blood
is
required
transfusions
for
fat
and
and
the
Kallikrein
Ka
fragments
LS:
5
–
10
days
Seal
blood
vessel
typical
transfusion
reaction
granules
prothrombin
activator
Cross-linked
fibrin
•promegakaryocyte,
Treated
with
whole
blood
transfusions
thrombin
activity
to
stimulate
bone
marrow
megakaryocyte,
and
platelets
•normal
Strengthens
and
stabilizes
the
clot
Platelet
phospholipid
transfusions
kidneys
activate
and
lymphocytes
causes
after
birth
renal
to
mount
failure
immune
response
PL
(inflammatory
chemical
as
VD,
attracts
WBCs
Home
Exit
drugs,
and
values
bone
marrow
transplants
tears
mainly
used
for
legalities
2
–
4
m
10
–
12
m
vitamin
injection
K
of
absorption
missing
factors
Fibrin BASIMFibrin
degradation
products (FDP)
ZWAIN
LECTURE
NOTES
2+
2+
2+
2+
2+