There's more to anaemia than iron deficiency...

Anaemia is the condition of having less than normal number of red blood cells or less than normal quantity of haemoglobin (Hb) in the blood.  The oxygen-carrying capacity of the blood is therefore decreased.  
Most, if not all of us, have had their Hb checked, at least once in our life. It stupefies me when people (some health workers included) relate all cases of low Hb to iron deficiency without first ascertaining the cause.
I recently carried out a Hb estimation for a nurse friend who rebuffed me and actually doubted my systems after the result showed no improvement from what it had been half a year earlier despite her increased intake of iron-rich foods. I really couldn't make out why she deemed herself immune from other types of anaemia. I thought she would consider taking further investigations after finding the level to be low a second time.Call it denial if you wish.
By the way, you may ingest good amounts of iron but have problems with its absorption.
Away from my friend now.
How many people with no medical training know that there exists anaemias other than iron-deficiency anaemia? This is the lot this article targets.
In a very simple language I give you a glimpse of some of the other anaemias they seldom mention in those consultation rooms.

Pernicious anaemia;
This is a chronic illness caused by impaired absorption of vitamin B12. It is a type of megaloblastic anaemia(red blood cells are abnormally large). Vitamin B12 is necessary in DNA synthesis during red cell formation. Lack of it leads to impaired DNA synthesis hence the megaloblastic changes. The causes of this malabsorption of  vitamin B12 may be:
1. Absence or lack of intrinsic factor (IF), a protein necessary in vitamin B12 absorption.
2. An autoimmune mechanism- an autoantibody  interfers with the normal uptake of vitamin B12. This vitamin is not absorbed directly but MUST first associate with a protein called intrinsic factor that is synthesized by the parietal cells in gastric mucosa. This vitamin-protein complex is then transported across the intestinal mucosa where absorption takes place. Plasma cells in the gastric mucosa of patients with pernicious anaemia secrete an autoantibody specific for intrinsic factor. This autoantibody combines with intrinsic factor thus inhibiting its role as a carrier for vitamin B12.
3. Infection with fish tapeworm;-there's competitive absorption of the host's vitaminB12.

Folate(folic acid) deficiency anemia;
It's a type of megaloblastic anemia. Folic acid is necessary for red blood cell formation(DNA synthesis by the highly dividing cells).
Causes; certain medications, chronic alcoholism, crohn's disease, celiac disease.
 Risk factors include;
1. Pregnancy- due to increased demand for folate
2. Eating over-cooked food.
3. Alcoholism- alcohol interferes with the absorption of folate.
4. Poor diet;- poverty-stricken, the elderly and people who do not eat fresh fruits and vegetables.


Autoimmune haemolytic anemias
These occur due to production of antibodies against a person's own red blood cells. These lead to destruction of one's red blood cells resulting in a crisis (shortage)

Haemolytic Disease of the Newborn due to ABO incompatibility

Forget about the overpublicized HDN due to Rhesus incompatibility and read about this one; 

It is an immune haemolytic anaemia which causes an infant to be born anaemic and jaundiced.
ABO HDN can occur when a group O mother with a high titre of immune IgG anti-A and anti-B (usually >1:64) in her serum becomes pregnant with a group A or group B infant.
IgG anti-A and anti-B cross the placenta and enter the foetal circulation causing destruction of foetal red cells.
Group B infants are often more severely affected than group A infants.

INVESTIGATIONS
1. ABO cell grouping of the infant using washed cord cells. When the infant is group A or group B carry out the following:

2. Maternal-infant ABO blood group incompatibility test as follows:
(i) pipette 2 volumes of fresh serum from the mother into a tube.
(ii) add 1 volume of infant's washed 5% cell suspension and mix.
(iii) incubate at 37 degrees Celsius for 15 minutes. Centrifuge at slow speed (150 rpm) for 1 minute.
(iv) examine the tube for haemolysis.
* Lysis of the red cells indicates ABO HDN.

3. Direct Coomb's Test (DCT) on the infant's red cells to check whether they have been coated with IgG antibody.

4. Check haemoglobin.

5. Check serum bilirubin of the infant.

6. Romanowsky-stained thin film--this shows spherocytosis which may be marked, polychromasia (due to reticulocytosis) and nucleated red cells.

NOTE:
*ABO HDN is rarely sufficiently severe to require exchange transfusion. In a situation in which it is indicated, group O blood (of the same Rhesus group as the infant) should be selected and cross matched with mother's serum.
*In contrast to Rhesus HDN, ABO HDN may occur in the first pregnancy and may not affect subsequent pregnancies depending on the ABO group of the infant.