Dr. Soban sadiq
Oral Therapy:
Ferrous Sulphate
Ferrous Fumarate
Ferrous Gluconate
Parenteral Therapy:
Iron Dextran
Iron-sucrose complex
Iron sodium gluconate complex
 Iron
deficiency anemia in
 Infants
 Pregnant and lactating women
 Children during rapid growth periods
Common adverse effects:
 Nausea
 Epigastric discomfort
 Abdominal cramps
 Constipation/diarrhea
These effects are usually dose-related and can often be
overcome by lowering the daily dose of iron or by taking the
tablets immediately after or with meals
Patients taking oral iron develop black stools; this has no
clinical significance in itself but may obscure the diagnosis of
continued gastrointestinal blood loss
Parenteral therapy should be reserved for patients who
are unable to tolerate or absorb oral iron and for
patients with extensive chronic blood loss .
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Postgastrectomy conditions
Small bowel resection
Inflammatory bowel disease(proximal small bowel)
Malabsorption syndromes
Essential in two reactions:
1. Conversion of methylmalonyl-coenzyme A
to Succinyl-CoA
2. Conversion of Homocysteine to Methionine
The second reaction is linked to folic acid
metabolism and synthesis of deoxythymidylate
(dTMP)
dTMP is a precursor for DNA synthesis
In Vitamin B12 deficiency, folate accumulates
as N-Methyltetrahydrofolate
The supply of tetrahydrofolate is depleted
This slows production of RBCs
Folic acid replacement can correct B12
deficiency anemia, but not the neurological
manifestation of B12 deficiency.
Absorption:
Vitamin B12 binds to Intrinsic factor (secreted by
gastric parietal cells)
It prevents digestion of B12
In bound state ,it binds to receptors on brush
border of mucosa
These receptors are located in ileum
Bound intrinsic factor and B12 are absorbed with
pinocytosis
DISTRIBUTION:
Vitamin B12 is distributed to various cells
bound to a plasma glycoprotein,Transcobalamin II
STORAGE:
Excess vitamin B12 (upto 300-500 microgram) is
stored in liver
ELIMINATION :
Trace amounts of vitamin B12 are normally lost
in urine and stool.
Significant amount of vitamin B12 are excreted
in urine (when large amounts are given
parenterally)
ABOSRPTION:
Form:
Dietary folates in polyglutamate forms; first
undergo hydrolysis by conjugase (present in
brush border of intestinal mucosa) and form
monoglutamate
Site:
Proximal jejunum
Only modest amounts of folic acid are stored in
body,therefore a decrease in diet will lead to
anemia in few months
Distribution:
Widely distributed through out the body via
blood stream
Storage:
Normally, 5-20 mg is stored in liver and other
tissues
Elimination:
Excreted in urine and stool, and also destroyed
by catabolism
These are used in anemia (megaloblastic)
Pernicious anemia ( Vitamin B12, basically IF)
Prophylaxis for neural tube defects (folic acid
before conception)
Neuropathy (Vitamin B12)
Cancer chemotherapy
Certain drug therapies lead to deficiency of folic
acid so replacement is required
Tablet and syrup forms:
Cyanocobalamin, Hydroxycobalamin
Parenteral:
I/M, I/V.
Use:
 To corrects major depletion of B12 quickly
 If patient is unable to take orally
 Required in patients with pernicious anemia(IF deficiency)
Parenteral therapy can lead to pain at injection site
Both are very well tolerated
There are no remarkable adverse effects of
therapy
 The
side effect which primarily limits
acceptability of oral iron therapy is
 Black
stools
 Epigastric pain and bowel upset
 Staining of teeth
 Metallic taste
 Choose
the correct statement about iron
therapy
 Iron
is given in megaloblastic anemia
 Iron must be given orally except in pernicious
anemia
 Prophylactic iron therapy must be given
during pregnancy
 Infants on breast feeding do not require
medicinal iron
A
23 year old pregnant woman is referred by
her obstetrician for evaluation of anemia.If
this woman has macrocytic anemia,an
increased serum concentration of vitamin
B12,the most likely cause of her anemia is
deficiency of ,
 Cobalamin
 Erythropoietin
 Folic acid
 Intrinsic factor
 Iron
 If
the patient had folic acid deficiency,her
infant would have a higher than normal risk
of
 Cardiac abnormality
 Kidney damage
 Limb deformity
 Neural tube defect
A
pregnant patient is found to have
microcytic anemia.Optimal treatment of
microcytic anemia is
A
high fibre diet
 Erythropoietin injections
 Ferrous sulphate tablet
 Folic acid supplements
 Hydroxocobalamin injections
 The
iron stored in intestinal mucosal cells is
complexed to
 Intrinsic
factor
 Transcobalamin II
 Transferrin
 Ferritin
 An
important biochemical consequence of
vitamin B12 deficiency is accumulation of
 Dihydrofolate
 dTMP
 Folic
acid
 Tetrahydrofolate
 Methyltetrahydrofolate

Mr. Abid, 25 years of age was suffering from
chronic lethargy and weakness On examination
he was very pale and he had signs of neuropathy
as well. His Laboratory tests showed
megaloblastic type of anemia. His physician
performed Schilling’s test, which was positive.
Choice of management would be:

Cyanocobalamin orally
 Folic acid orally
 Vitamin B12, I/V
 Folic acid+Vitamin B12 orally
 Intrinsic factor orally
