638
UNIT 4
Maintenance of the Body
17
Two B-complex vitamins—vitamin B
12
and folic acid—are
necessary for normal DNA synthesis. Even slight deficits jeop-
ardize rapidly dividing cell populations, such as developing
erythrocytes.
Fate and Destruction of Erythrocytes
Red blood cells have a useful life span of 100 to 120 days. ±eir
anucleate condition carries with it some important limitations.
Red blood cells are unable to synthesize new proteins, grow, or
divide. Erythrocytes become “old” as they lose their flexibility, be-
come increasingly rigid and fragile, and their hemoglobin begins
to degenerate. ±ey become trapped and fragment in smaller cir-
culatory channels, particularly in those of the spleen. For this rea-
son, the spleen is sometimes called the “red blood cell graveyard.”
We will briefly describe the fate of aged and damaged eryth-
rocytes here, but Figure 17.7 gives a more detailed account.
Macrophages engulf and destroy dying erythrocytes. ±e heme
of their hemoglobin is split off from globin. Its core of iron is
salvaged, bound to protein (as ferritin or hemosiderin), and
stored for reuse. ±e balance of the heme group is degraded to
bilirubin
(bil
0
ĭ-roo
9
bin), a yellow pigment that is released to
the blood and binds to albumin for transport. Liver cells pick up
bilirubin and in turn secrete it (in bile) into the intestine, where
it is metabolized to
urobilinogen
. Most of this degraded pigment
leaves the body in feces, as a brown pigment called
stercobilin
.
±e protein (globin) part of hemoglobin is metabolized or bro-
ken down to amino acids, which are released to the circulation.
Erythrocyte Disorders
Most erythrocyte disorders can be classified as anemia or poly-
cythemia. We describe some of the many varieties and causes of
these conditions next.
Anemia
Anemia
(ah-ne
9
me-ah; “lacking blood”) is a condi-
tion in which the blood’s oxygen-carrying capacity is too low to
support normal metabolism. It is a
sign
of some disorder rather
than a disease in itself. Its hallmark is blood oxygen levels that
are inadequate to support normal metabolism. Anemic indi-
viduals are fatigued, o²en pale, short of breath, and chilled.
±e causes of anemia can be divided into three groups: blood
loss, not enough red blood cells produced, or too many of them
destroyed.
Blood loss.
Hemorrhagic anemia
(hem
0
o-raj
9
ik) is caused by
blood loss. In acute hemorrhagic anemia, blood loss is rapid
(as might follow a severe stab wound); it is treated by replac-
ing the lost blood. Slight but persistent blood loss (due to
hemorrhoids or an undiagnosed bleeding ulcer, for exam-
ple) causes chronic hemorrhagic anemia. Once the primary
problem is resolved, normal erythropoietic mechanisms re-
place the lost blood cells.
Not enough red blood cells produced.
A number of prob-
lems can decrease erythrocyte production. ±ese problems
range from lack of essential raw materials (such as iron) to
complete and utter failure of the red bone marrow.
Iron-deficiency anemia
is generally a secondary result of
hemorrhagic anemia, but it also results from inadequate
Low O
2
levels in blood stimulate
kidneys to produce erythropoietin.
1
Erythropoietin levels rise in blood.
2
Erythropoietin and necessary raw
materials in blood promote
erythropoiesis in red bone marrow.
3
Aged and damaged
red blood cells are engulfed by
macrophages of spleen, liver, and
bone marrow; the hemoglobin is
broken down.
5
New erythrocytes
enter bloodstream;
function about 120
days.
4
Raw materials are made
available in blood for
erythrocyte synthesis.
6
Hemoglobin
Amino
acids
Globin
Iron is bound to transferrin
and released to blood
from liver as needed
for erythropoiesis.
Heme
Circulation
Iron is stored
as ferritin or
hemosiderin.
Bilirubin is secreted into
intestine in bile where it is
metabolized to stercobilin
by bacteria.
Stercobilin
is excreted
in feces.
Bilirubin is
picked up
by the liver.
Food nutrients
(amino acids, Fe,
B
12
, and folic acid)
are absorbed from
intestine and enter
blood.
Figure 17.7
Life cycle of red blood cells.
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