Blood Composition
Bodys only fluid tissue
Composed of liquid plasma and
formed elements
Formed elements include:
Erythrocytes, or red blood cells
(RBCs)
Leukocytes, or white blood cells
(WBCs)
Platelets
Plasma
92% water
8% proteins
Albumins
Globulins
Immunoglobulins
Transport globulins
Fibrinogen
Components of Whole Blood
Functions of Blood
Transportation
Substance 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
Regulate blood levels of
particular substances
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
Protection of body
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
Formed Elements
Red Blood Cells
Also known as erythrocytes
Biconcave disc
Anucleate
RBCs have no nuclei or organelles
Filled with hemoglobin (Hb), a
protein that functions in gas transport
Contain the plasma membrane
protein spectrin and other proteins that:
Give erythrocytes their
flexibility
Allow them to change shape as
necessary
Large surface area/volume
Biconcave shape has a huge surface
area relative to volume
Hemoglobin
Hematocrit
The percentage of RBCs out of the
total blood volume
RBCs are dedicated to respiratory
gas transport
Erythrocytes are more than 97%
hemoglobin
Hb reversibly binds with oxygen
and most oxygen in the blood is bound to Hb
ATP is generated anaerobically, so
the erythrocytes do not consume the oxygen they transport
Hb 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 to one oxygen molecule
Each Hb molecule can transport
four molecules of oxygen
Structure of Hemoglobin
Hemoglobin (Hb)
Oxyhemoglobin Hb bound to oxygen
Oxygen loading takes place in the lungs
Deoxyhemoglobin Hb after oxygen
diffuses into tissues (reduced Hb)
Carbaminohemoglobin Hb bound to carbon
dioxide
Carbon dioxide loading takes place in the
tissues
RBC Formation
Erythropoiesis
Circulating erythrocytes the
number remains constant and reflects a balance between RBC production and
destruction
Too few RBCs leads to tissue
hypoxia
Hypoxia is when tissues are
exposed to low levels of oxygen
Too many RBCs 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
Erythropoietin Mechanism
RBC Recycling
The life span of an erythrocyte is
100120 days
Old RBCs become rigid and fragile,
and their Hb begins to degenerate
Dying RBCs are engulfed by
macrophages
Hb has to be broken apart
Heme and globin are separated and
the iron is salvaged for reuse
Transferrin
Globulins
Globin is metabolized into amino
acids and is released into the circulation
Heme
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 brown pigment called stercobilin
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: Decreased Hemoglobin Content
Iron-deficiency anemia results
from:
Inadequate intake of
iron-containing foods
Impaired iron absorption
Pernicious anemia results from:
Deficiency of vitamin B12
Lack of intrinsic factor needed
for absorption of B12
Treatment is intramuscular
injection of B12 or application of Nascobal (gel)
Other Erythrocyte Disorders
Sickle-cell anemia results from a
defective gene coding for an abnormal Hb called hemoglobin S (HbS)
This defect causes RBCs to become
sickle-shaped in low oxygen situations
Polycythemia excess RBCs that increase
blood viscosity
Blood doping
Banned from Olympic Games
White Blood Cells
Also know as leukocytes
The only blood components that are
complete cells
Possess nuclei and organelles
Protect body against invasion
Characteristics
Amoeboid movement
Can leave capillaries via
diapedesis
Move through tissue spaces
Positive chemotaxis
Some are capable of phagocytosis
Leukocytosis WBC count over
11,000 / mm3
Normal response to bacterial or
viral invasion
Granulocytes
Are all phagocytic cells
Eosinophils
Lead the bodys counterattack
against parasitic worms
Basophils
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 (antihistamines counter this
effect)
Neutrophils
Are our bodys bacteria slayers
Agranulocytes
Lack visible cytoplasmic granules
Lymphocytes
Two types:
T cells function in the immune
response
B cells give rise to plasma cells,
which produce antibodies
Monocytes
Largest leukocytes
They leave the circulation, enter
tissue, and differentiate into macrophages
Macrophages
Are highly mobile and actively
phagocytic
Activate lymphocytes to mount an
immune response
Percentages of Leukocytes
PLATELETS
Fragments of megakaryocytes (red
bone marrow cells)
Function in the clotting mechanism
Transport chemicals
Form a temporary platelet plug
that helps seal breaks in blood vessels
Contraction after clot formation
HEMOSTASIS
A series of reactions for stoppage of
bleeding
During hemostasis, three phases occur in
rapid sequence
1) Vascular spasm
Vascular spasms immediate
vasoconstriction in response to injury
Release signals
HEMOSTASIS
2) Platelet plug formation
Platelets do not stick to each other or
to blood vessels
Upon damage to blood vessel endothelium
platelets:
With the help of von Willebrand factor
(VWF) adhere to collagen
Stick to exposed collagen fibers and form
a platelet plug
Release serotonin and ADP, which attract
still more platelets
HEMOSTASIS
3) Coagulation (blood clotting)
Follows intrinsic and extrinsic
pathways
Clotting factors
Each pathway cascades toward
factor X
Once factor X has been activated,
it complexes with factor V to form prothrombin activator
Extrinsic pathway
Tissue factor (III)
ΰ
X + V ΰ
prothrombin activator
Intrinsic pathway
XII
ΰ
X + V ΰ
prothrombinase
Common pathway
Prothrombin activator is formed
Prothrombin activator catalyzes
the transformation of prothrombin to the active enzyme thrombin
Prothrombin
ΰ
thrombin (Prothrombin is converted into thrombin)
Fibrinogen
ΰ
fibrin (Thrombin catalyzes the joining of fibrinogen into a fibrin mesh)
Insoluble fibrin strands form the
structural basis of a clot
Detailed Events of Coagulation
HEMOSTASIS
Calcium ions & vitamin K
Fibrin in the presence of calcium
ions strengthens and stabilizes the clot
Clot retraction
Stabilization of the clot
Fibrinolysis
Plasminogen
ΰ
plasmin
Blood Types
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 or absence of these
antigens is used to classify blood groups
The antigens of the ABO and Rh
blood groups cause vigorous transfusion reactions when they are improperly
transfused
ABO Blood Groups