Book of Medical Disorders in Pregnancy - Tintash

pregnancy and labour. The monthly
blood loss in women averages 50 ml
corresponding to 25 mg of hemoglobin
iron. There is considerable iron loss
during child bearing in spite of abeyance
in menstruation.
The main iron demands of the mother
start in the last two months of pregnancy
when the fetus and placenta are growing
rapidly, this is followed by the blood
loss during labor. Anaemia for lack of
iron commonly develops during pregnancy.
Iron absorption:
Very little is known about the changes
which food iron undergoes in the
alimentary canal. It is believed that
inorganic iron is split off from ferritin,
(Tissue iron storage compound) but the
digestive juices cannot release the iron
which is bound with the porphyrin
molecule in the heme compounds of
food.
Iron is absorbed in the ferrous form
possibly in the stomach and certainly in
the duodenum and upper small intestine.
The presence of bile salts does not
promote iron absorption. The iron is
taken up by the cells of the intestinal
mucosa and combines with apoferritin
there to form ferritin, which releases its
contained iron into the circulation when
required for hemoglobin formation. It is
found clinically that a total iron food
intake of 10 to 15 mg daily is sufficient
to maintain a normal state of the blood in
all physiological states in women and
children and is well above the minimal
requirements of normal man. Normal
gastric acidity is important in favoring
the absorption. Iron is absorbed in the
first portion of the duodenum chiefly as
the ferrous salt. At the low ph of the
stomach the colloidal ferric iron of food
is changed to monomolecular ferric iron,
and is then reduced by foodstuffs to the
more soluble ferrous state for absorption.
Once in the mucosal epithelial cell, most
is again oxidized to the ferric state. The
mechanisms which control the rate of
absorption are still somewhat
controversial. One of the most widely
accepted views, the mucosal block
theory, postulates that the rate of
absorption depends upon the degree of
unsaturation of the apoferritin in the
duodenal lining epithelium. Iron is
absorbed into the intestinal mucosa cells
after reduction to the ferrous state, and
conjugates there with apoferritin to form
ferritin. When the apoferritin is
completely saturated and totally
transformed to ferritin, further
absorption is blocked. The various body
needs are supplied by the release of the
iron from the ferritin complex, thus
producing more unsaturated apoferritin
available for combination with iron.
The release of iron from the ferritin
complex appears to be a function of the
oxygen carrying capacity of the blood.
When the hemoglobin level of the blood
is low, the oxygen level is depressed,
and more iron is transferred from the
ferritin molecule in the cells of the
intestinal mucosa to siderophilin (Tran’s
ferritin) in the serum. This mechanism
permits further absorption of iron into
the mucosal cells, to desaturate the
newly released apoferritin. It is also
suggested that there may be a direct
transfer of iron through the mucosal
cells, dependent upon oxidation
reduction potentials in these cells. This
direct transfer is particularly operative in
anaemic states where the anaerobic state
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