Pharmacology for Dentistry

(Ben Green) #1
248 Section 6/ Drug Acting on Blood

of which 66% is in haemoglobin and 25% is
stored as ferritin and hemosiderin and rest
is in muscles and enzyme.


Iron absorption occurs predominantly in
the duodenum and upper jejunum. The
physical state of iron entering the duodenum
greatly influences its absorption. At
physiological pH, ferrous iron is rapidly
oxidized to the insoluble ferric form. Gastric
acid lowers the pH in the proximal duodenum,
enhancing the solubility and uptake of ferric
iron. When gastric acid production is
impaired, iron absorption is reduced subs-
tantially. Ascorbic acid enhances iron
absorption. Ascorbic acid mobilizes iron from
iron-binding proteins in vivo, which in turn
could catalyze lipid peroxidation. Iron
absorption is inhibited by antacids, phytates,
phosphates and tetracyclines.


The iron is transferred by the mucosal
epithelium to the body and is bound to plasma
transferrin in the ferric state. In the plasma, iron
takes part in a dynamic transferrin-iron
equilibrium and is distributed into vascular and
interstitial extravascular compartment. 50 to
60% of transferrin is extravascular. The plasma
iron pool in adults is about 3 mg and has an
estimated turnover of 20 to 30 mg per 24 hours.
Daily and obligatory losses of iron in healthy
men are about 1 mg; in healthy menstruating
women these average 2 mg and in either case
are compensated by a net absorption of 1 to 2
mg from the intestine, which enters the mobile
pool of transferrin iron.


Pharmacokinetics


After oral administration iron is absorbed
in ferrous form. The conversion of ferric iron
to ferrous iron is aided by hydrochloric acid.


Iron is transported via transferrin. When
body stores of iron are high, ferric iron
combines with apoferritin to form ferritin.
Ferritin is the protein of iron storage. About
80 percent iron in plasma goes to erythroid
marrow. The excretion of iron is minimal.
Only little amount of iron is lost by exfoliation
of intestinal mucosal cells and trace amount
is excreted in urine, sweat and bile.
After confirmation of iron deficiency
iron therapy can be given by oral or
parenteral route. Generally oral iron therapy
is given unless the patient is suffering from
severe anaemia, malabsorption syndrome,
gastrectomy or patient is showing adverse
effects to oral iron therapy.

Uses
Nutritional iron deficiency anaemia; other
causes in which iron deficiency can occur are
pregnancy, lactation, infants, children. In
patients with malabsorption syndrome,
patients who are taking NSAIDs for long
period, patients with chronic inflammatory
disease and in patients of gastrectomy.
Preparations of iron alone or in
combination with vitamin B 12 , folic acid or
other vitamins are available (see table 6.2.1).
Most of the oral formulations contain
one of the iron compound with many
vitamins, amino acids, liver extract,
minerals, folic acid, appetite stimulants
(cyproheptadine like compound).

Adverse Effects
Oral administration can cause nausea,
vomiting, epigastric pain, metallic taste,
staining of teeth, constipation and diarrhoea
both can occur, but constipation is more
common.
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