Life Span of the White Blood Cells

Genesis of the White Blood Cells
Early differentiation of the pluripotential hematopoietic
stem cell into the different types of committed
stem cells is shown in Figure 32–2 in the previous
chapter. Aside from those cells committed to form red
blood cells, two major lineages of white blood cells are
formed, the myelocytic and the lymphocytic lineages.
The left side of Figure 33–1 shows the myelocytic
lineage, beginning with the myeloblast; the right
shows the lymphocytic lineage, beginning with the
lymphoblast.
Life Span of the White Blood Cells
The life of the granulocytes after being released from
the bone marrow is normally 4 to 8 hours circulating
in the blood and another 4 to 5 days in tissues where
they are needed. In times of serious tissue infection,
this total life span is often shortened to only a few
hours because the granulocytes proceed even more
rapidly to the infected area, perform their functions,
and, in the process, are themselves destroyed.
The monocytes also have a short transit time, 10 to
20 hours in the blood, before wandering through the
capillary membranes into the tissues. Once in the
tissues, they swell to much larger sizes to become tissue
macrophages, and, in this form, can live for months
unless destroyed while performing phagocytic functions.
These tissue macrophages are the basis of the
tissue macrophage system, discussed in greater detail
later, which provides continuing defense against
infection.
Lymphocytes enter the circulatory system continually,
along with drainage of lymph from the lymph
nodes and other lymphoid tissue. After a few hours,
they pass out of the blood back into the tissues by diapedesis.
Then, still later, they re-enter the lymph and
return to the blood again and again; thus, there is continual
circulation of lymphocytes through the body.
The lymphocytes have life spans of weeks or months;
this life span depends on the body’s need for these
cells.
The platelets in the blood are replaced about once
every 10 days; in other words, about 30,000 platelets
are formed each day for each microliter of blood.
Neutrophils and Macrophages
Defend Against Infections
It is mainly the neutrophils and tissue macrophages
that attack and destroy invading bacteria, viruses, and
other injurious agents. The neutrophils are mature
cells that can attack and destroy bacteria even in the
circulating blood. Conversely, the tissue macrophages
begin life as blood monocytes, which are immature
cells while still in the blood and have little ability to
fight infectious agents at that time. However, once they
enter the tissues, they begin to swell—sometimes
increasing their diameters as much as fivefold—to as
great as 60 to 80 micrometers, a size that can barely be
seen with the naked eye. These cells are now called
macrophages, and they are extremely capable of combating
intratissue disease agents.

Effect of Polycythemia on Function of the Circulatory System

Because of the greatly increased viscosity of the blood
in polycythemia, blood flow through the peripheral
blood vessels is often very sluggish. In accordance with
the factors that regulate return of blood to the heart,
as discussed in Chapter 20, increasing blood viscosity
decreases the rate of venous return to the heart. Conversely,
the blood volume is greatly increased in polycythemia,
which tends to increase venous return.
Actually, the cardiac output in polycythemia is not far
from normal, because these two factors more or less
neutralize each other.

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The arterial pressure is also normal in most people
with polycythemia, although in about one third of
them, the arterial pressure is elevated.This means that
the blood pressure–regulating mechanisms can usually
offset the tendency for increased blood viscosity to
increase peripheral resistance and, thereby, increase
arterial pressure. Beyond certain limits, however, these
regulations fail, and hypertension develops.
The color of the skin depends to a great extent on
the quantity of blood in the skin subpapillary venous
plexus. In polycythemia vera, the quantity of blood in
this plexus is greatly increased. Further, because the
blood passes sluggishly through the skin capillaries
before entering the venous plexus, a larger than
normal quantity of hemoglobin is deoxygenated. The
blue color of all this deoxygenated hemoglobin masks
the red color of the oxygenated hemoglobin. Therefore,
a person with polycythemia vera ordinarily has a
ruddy complexion with a bluish (cyanotic) tint to the
skin.

Polycythemia

Secondary Polycythemia. Whenever the tissues become
hypoxic because of too little oxygen in the breathed
air, such as at high altitudes, or because of failure of
oxygen delivery to the tissues, such as in cardiac
failure, the blood-forming organs automatically
produce large quantities of extra red blood cells. This
condition is called secondary polycythemia, and the
red cell count commonly rises to 6 to 7 million/mm3,
about 30 per cent above normal.
A common type of secondary polycythemia, called
physiologic polycythemia, occurs in natives who live at
altitudes of 14,000 to 17,000 feet, where the atmospheric
oxygen is very low.The blood count is generally
6 to 7 million/mm3; this allows these people to perform
428 Unit VI Blood Cells, Immunity, and Blood Clotting
reasonably high levels of continuous work even in a
rarefied atmosphere.
Polycythemia Vera (Erythremia). In addition to those
people who have physiologic polycythemia, others
have a pathological condition known as polycythemia
vera, in which the red blood cell count may be 7 to 8
million/mm3 and the hematocrit may be 60 to 70 per
cent instead of the normal 40 to 45 per cent. Polycythemia
vera is caused by a genetic aberration in the
hemocytoblastic cells that produce the blood cells.The
blast cells no longer stop producing red cells when too
many cells are already present.This causes excess production
of red blood cells in the same manner that a
breast tumor causes excess production of a specific
type of breast cell. It usually causes excess production
of white blood cells and platelets as well.
In polycythemia vera, not only does the hematocrit
increase, but the total blood volume also increases, on
some occasions to almost twice normal.As a result, the
entire vascular system becomes intensely engorged. In
addition, many blood capillaries become plugged by
the viscous blood; the viscosity of the blood in polycythemia
vera sometimes increases from the normal of
3 times the viscosity of water to 10 times that of water.

Life Span and Destruction of Red Blood Cells

When red blood cells are delivered from the bone
marrow into the circulatory system, they normally circulate
an average of 120 days before being destroyed.
Even though mature red cells do not have a nucleus,
mitochondria, or endoplasmic reticulum, they do have
cytoplasmic enzymes that are capable of metabolizing
glucose and forming small amounts of adenosine
triphosphate.These enzymes also (1) maintain pliability
of the cell membrane, (2) maintain membrane
transport of ions, (3) keep the iron of the cells’ hemoglobin
in the ferrous form rather than ferric form, and
(4) prevent oxidation of the proteins in the red cells.
Even so, the metabolic systems of old red cells become
progressively less active, and the cells become more
and more fragile, presumably because their life
processes wear out.
Once the red cell membrane becomes fragile, the
cell ruptures during passage through some tight spot
of the circulation. Many of the red cells self-destruct
in the spleen, where they squeeze through the red pulp
of the spleen.There, the spaces between the structural
trabeculae of the red pulp, through which most of the
cells must pass, are only 3 micrometers wide, in comparison
with the 8-micrometer diameter of the red
cell. When the spleen is removed, the number of old
abnormal red cells circulating in the blood increases
considerably.

Anemias

Anemia means deficiency of hemoglobin in the blood,
which can be caused by either too few red blood cells
or too little hemoglobin in the cells. Some types of
anemia and their physiologic causes are the following.
Blood Loss Anemia. After rapid hemorrhage, the body
replaces the fluid portion of the plasma in 1 to 3 days,
but this leaves a low concentration of red blood cells.
If a second hemorrhage does not occur, the red blood
cell concentration usually returns to normal within 3
to 6 weeks.
In chronic blood loss, a person frequently cannot
absorb enough iron from the intestines to form hemoglobin
as rapidly as it is lost. Red cells are then produced
that are much smaller than normal and have too
little hemoglobin inside them, giving rise to microcytic,
hypochromic anemia, which is shown in Figure 32–3.
Aplastic Anemia. Bone marrow aplasia means lack of
functioning bone marrow. For instance, a person
exposed to gamma ray radiation from a nuclear bomb
blast can sustain complete destruction of bone
marrow, followed in a few weeks by lethal anemia.
Likewise, excessive x-ray treatment, certain industrial
chemicals, and even drugs to which the person might
be sensitive can cause the same effect.

Megaloblastic Anemia. Based on the earlier discussions
of vitamin B12, folic acid, and intrinsic factor from the
stomach mucosa, one can readily understand that loss
of any one of these can lead to slow reproduction of
erythroblasts in the bone marrow. As a result, the red
cells grow too large, with odd shapes, and are called
megaloblasts. Thus, atrophy of the stomach mucosa,
as occurs in pernicious anemia, or loss of the entire
stomach after surgical total gastrectomy can lead to
megaloblastic anemia. Also, patients who have intestinal
sprue, in which folic acid, vitamin B12, and other
vitamin B compounds are poorly absorbed, often
develop megaloblastic anemia. Because in these states
the erythroblasts cannot proliferate rapidly enough to
form normal numbers of red blood cells, those red cells
that are formed are mostly oversized, have bizarre
shapes, and have fragile membranes. These cells
rupture easily, leaving the person in dire need of an
adequate number of red cells.