Professional Documents
Culture Documents
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Physical characteristics of blood
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Functions of Blood
Transportation
O2/CO2; nutrients/wastes; enzymes; hormones
Regulation
body temperature; pH & ion composition of interstitial
fluid; intracellular fluid volume
Protection
defense against pathogens; restriction of fluid loss at
injury sites
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Composition of Blood
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Plasma
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Formed Elements
granular
agranular
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Hemopoiesis
Megakaryoblast
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Erythrocytes (RBCs)
Biconcave shape, flexible cells
around 5 million RBCs per mm3 blood
average “life span” of 120 days
Cells
contains cytosol, no nucleus/organelles; filled with
Hemoglobin (Hb)
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Hemoglobin
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As RBCs get damaged/worn out, they must be
removed from circulation & replaced
About 1% of the circulating RBCs are replaced
each day, at at rate of about 3 million RBCs per
second
Worn out RBCs are removed by phagocytic cells
in the liver, spleen & bone marrow
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Hemoglobin recycling
“globin” proteins will be
broken down into amino acids
to be re-used by cells to make
new proteins
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Erythropoiesis
The formation of RBCs
Occurs in bone marrow
(myeloid tissue) due to
hypoxia detected in kidneys
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Blood Typing
There are many different surface antigens
(transmembrane proteins) within the plasma membrane of
your RBCs. These antigens (a.k.a. “agglutinogens”) are
genetically determined.
Yoursurface antigens are recognized by your immune
defense system as “self”.
The presence or absence of 3 specific antigens (A, B &
Rh) determine your “blood type”
Within your plasma, you may have specific antibodies
(a.k.a. “agglutinins”) against surface antigens that are not
yours.
Plasma antibodies are responsible for “protecting” you
from
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an incompatible blood type
Blood Typing
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Blood Typing
When you combine the information from the AB & Rh
antigens, the possible blood types will be:
A+/A-
B+/B-
AB+/AB-
O+/O-
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Blood Typing
Unlike the AB grouping, people who are Rh- do not
genetically create antibodies against Rh in their plasma.
Antibodies will only be formed after an initial exposure to Rh
This could happen during an incompatible transfusion (i.e.
A+ A- ), or during pregnancy if an Rh- mom is carrying an
Rh+ baby.
Rh antibody formation in a mom who is carrying an Rh+
baby will lead to “hemolytic disease of the newborn”
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Leukocytes (WBCs)
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Differential Count & Functions of WBCs
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Differential Count & Functions of WBCs
Neutrophils - 50-70%
function in acute bacterial infections; phagocytic
Lymphocytes – 20-30%
function in “immunity” – specific resistance to disease
Monocytes – 4-8%
function in chronic bacterial infections; migrate into
tissues to become “wandering macrophages”
Eosinophils – 2-4%
active against parasites & elevated in allergic reactions;
destroy antibody-coated antigens by phagocytosis
Basophils - <1%
release chemicals (histamine, heparin) during tissue
inflammation
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Immunity ( Chap 14, p. 464-471)
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Overview of Immunity
Fig. 14-11)
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Immunity is either “innate” or “acquired”
Innate Immunity
present at birth
independent of previous
exposure to Ag
genetically determined
species dependent
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Acquired Immunity
arises throughout life by active or passive means
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Active immunity – development of resistance (i.e.
antibody (Ab) production) to specific disease
secondary to exposure to specific Ag (pathogen)
naturally acquired active immunity – natural exposure
results in immune response & development of long term
immunity
induced (artificial) active immunity – deliberate “artificial”
exposure to Ag (i.e. vaccine/immunization)
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Passive immunity – development of immunity due to
transfer of “pre-made” antibodies
naturally acquired passive immunity – Ab’s transferred from
mom baby across placenta or in breast-milk
induced (artificial) passive immunity – administration of Ab’s
to fight disease after exposure to pathogen
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Properties of Immunity
Immunity has four general properties:
Specificity
Versatility
Memory
Tolerance
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Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Properties of Immunity
Specificity – T & B cells have specific receptors that will
allow them to only recognize & target a specific Ag; this
process is known as “antigen recognition”
Versatility – millions of different lymphocyte populations,
each with specific Ag recognizing receptors; allows for
“anticipation” of potential Ag’s
Memory – after initial exposure, long term acquired
immunity occurs through the production of memory cells;
secondary exposure results in stronger faster response to
previously recognized Ag
Tolerance – immune cells recognize self-antigens &
“tolerate” (ignore) them, only going after foreign (non-self)
Ag’s
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Overview of the immune response
The purpose of the immune response is to inactivate or
destroy pathogens, abnormal cells & foreign molecules (such
as toxins)
In order for the response to occur, lymphocytes must be
“activated” by the process of antigen recognition
T cells are usually activated first, & then B cells. T cells mainly
rely on activation by phagocytic cells collectively known as
“antigen presenting cells (APC’s)”
Once activated, T cells both attack the invader, & stimulate
the activation of B cells
Activated B cells mature into “plasma cells” which produce
specific antibodies designed to inactivate the harmful antigen.
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Cell Mediated (a.k.a. Cellular) Immunity
In order for T cells to respond, they must first be activated by
exposure to an antigen which is bound to membrane receptors of
phagocytic antigen presenting cells (APC’s) (“antigen recognition”)
These membrane receptors on cells are called “MHC proteins”
(major histocompatibility complex proteins), & are genetically
determined (i.e. differ among individuals)
Antigens bound to MHC proteins “tell” the T lymphocyte what the
specific foreign invader is (i.e. a specific bacteria) so that the
lymphocytes can mount a cellular defense
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Cell Mediated (a.k.a. Cellular) Immunity
Once a T cell is activated by the presentation of the combined
MHC/Ag, it will clone (by mitosis) & differentiate into:
cytotoxic T cells – seek out the specific
pathogen/infected cell that contains the targeted Ag &
destroys it by secreting various chemicals
helper T cells – necessary for coordination of both
specific & non-specific defenses, as well as for stimulating
both cell-mediated & antibody-mediated immunity.
In cell-mediated immunity they release chemicals
(cytokines) that strengthen the activity of cytotoxic T
cells.
In antibody-mediated immunity they release cytokines
that stimulate activated B cell division & differentiation
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Cell Mediated (a.k.a. Cellular) Immunity
memory T cells – remain “in reserve” so if same Ag
appears, these cells can immediately differentiate into
cytotoxic & helper T cells, causing a swift secondary
response to the invasion
suppressor T cells – activated more slowly than the other T
cells; inhibit the response of the immune cells to prevent
potential “autoimmune” response
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Activated T cells clone &
differentiate into:
Cytotoxic T cells
Direct physical &
Helper T cells
chemical attack
Memory T cells
Suppressor T cells
Antigens
viruses
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Antibody Mediated (Humoral) Immunity
B cells must also be activated before they can respond to an
invading Ag
The body has millions of different B cell populations, each B
cell has its own particular antibody (Ab) molecule within its
cell membrane
When the corresponding Ag invades the interstitial fluid
surrounding the B cell, the Ag binds to the Ab & is taken into
the cell, eventually being displayed on the B cell’s MHC
protein. The B cell is now “sensitized”
Helper T cells (that had been previously activated to the
same Ag) then attach to the sensitized B cells & activate them
by secreting chemicals (cytokines)
Cytokine secretion results in B cell cloning & differentiation
into plasma cells & memory cells
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Antibody Mediated (Humoral) Immunity
Plasma cells produce millions of copies of antibodies which
are released into the blood & lymph
Antibodies seek out & bind to the Ag forming an “Ab-Ag
complex”, eventually leading to the elimination of the antigen
by various means
Memory cells remain in reserve to respond to any
subsequent exposure by the same Ag. Upon secondary
exposure, memory B cells quickly differentiate into Ab
producing plasma cells
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Antibody Mediated (Humoral) Immunity
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Antibody Mediated (Humoral) Immunity
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Review of Immune Response
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Platelets (Thrombocytes)
Cellular fragments (cell membrane “packet” filled with
cytoplasm) from large Megakaryocytes found within bone
marrow
around 350,000 platelets/mm3
platelets circulate for 9-12 days before being removed
from circulation
platelets function in “hemostasis” – the processes that stop
bleeding from damaged blood vessels
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Hemostasis
There are three overlapping processes of hemostasis:
1. Vascular spasm – damage to BV wall causes the smooth
muscle within the wall to spasm vasoconstriction &
decreased blood loss through vessel; begins within a few
seconds of injury, lasts about 30 minutes
2. Platelet plug formation – damaged BV endothelium gets
sticky & circulating platelets stick to the endothelium & each
other, creating a platelet plug; begins within 15 seconds of
BV damage; may be enough to stop bleeding completely
within a small BV (i.e. capillary)
3. Coagulation – blood clotting; complex series of steps
resulting in the conversion of fibrinogen fibrin
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Overview of Coagulation
• initiated by both
“extrinsic” (tissue) &
“intrinsic” (platelet) factors
•both pathways result in
activation of Factor X (10)
•activation of Factor X
begins the “common
pathway”
•all 3 pathways require
the presence of Ca2+ &
vitamin K
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Coagulation
Extrinsic pathway –
begins with damage to surrounding tissues & BV
endothelium which cause the release of “tissue factors”
eventually results in the formation of an enzyme (“Factor X
activator”) capable of activating Factor X
shorter, quicker pathway for initiation of coagulation
Intrinsic pathway –
begins with the release of “platelet factors”
eventually results in the formation of “Factor X activator”
more complicated, slower pathway of coagulation
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Coagulation
Common pathway –
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Clot Retraction, Repair & Removal
Once the clot has begun to form, the fibrin threads &
trapped platelets cause the edges of the damaged vessel to
pull together causing “clot retraction”
Repair to the damage vessel & surrounding tissues occur as
fibroblasts invade the area & endothelial cells regenerate
Eventually the clot gets removed by the enzyme “plasmin” in
a process known as “fibrinolysis”
A clot which remains present in an intact vessel is known as
a “thrombus”. Thrombi can block blood flow & pieces can
dislodge creating an “embolism”
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