Essay on “Anaemia” (1016 Words)

Worldwide anaemia is the commonest red cell disorder. Anaemia leads to a decreased amount of haemoglobin concentration, red cell count and PCV value. The anaemia is present when Hb concentration falls below in the following:

Newborn infants – 14 g/ dl

Child 6 months to 4 year – 11 g/ dl

Child 5 to 11 year – 11.5 g/dl

Child 12 to 14 year – 12.0 g/dl

Non-pregnant women – 12.0 g/dl

Pregnant women – 11.0 d/dl

Men /adult boys – 13.0 g/dl

In tropical and developing countries anaemia is seen in 50% or more of pre-school children and in pregnant women, it is moderate or severe. The main causes of anaemia includes malnutrition, protein deficiency, folate deficiency, parasitic, bacterial and viral infections, or it may be inherited.

Classification:

Anaemias may be classified in two ways:

a. Based upon morphology of red cell or

b. Upon the aetiology, i.e. the cause of anaemia.

Based upon Morphological Classification:

It is based on MCV, MCH, MCHC and the red cell morphology on a blood smear.

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Normochromic Normocytic Anaemia:

In this type of anaemia, RBCs are normal in size and colour, but reduced in number. The packed cell volume is reduced. MCH, MCV, and MCHC are normal. Normocytic normo­chromic anaemia may be found in acute blood loss, Anaemia of chronic disease aplastic anaemia.

Hypochromic Microcytic Anaemia:

The red cells are small and pale. Decrease in total RBC count, low Hb and PCV, reduced MCV, MCH and MCHC; Hypochromic microcytic anaemia is found in iron deficiency anaemia and thalassemia.

Normochromic Macrocytic Anaemia:

The red cells are larger in size with no central pale portion. RBC are reduced in number with low Hb, elevated MCV and MCH and normal MCHC. Normochromic macrocytic anaemia is found in pernicious anaemia, anaemia of folic acid and vitamin B₁₂ deficiency and in some cases of aplastic anaemia.

Normochromic Microcytic Anaemia:

The RBC are small in size with low Hb, reduced MCV, MCH and normal MCHC. This type of anaemia is found in some of the anaemias of chronic infections (Fig. 20.1, Plate 1).

Aetiological Classification:

Based upon the cause of anaemia, following types of anaemia are found.

Aplastic Anaemia:

It may occur due to congenital defect, i.e. chromosomal abnormalities in RBC or exposure to various physical and chemical reagents like insecticides, streptomycin, ionizing radiation, etc. Usually RBCs are normal. But, sometimes aniso- cytosis or poikilocytosis may be seen. Decreased WBC counts decreased platelets.

Bleeding time is increased. Bone marrow is aplastic. Rapid ESR. Aplastic anaemia may terminate as leukaemia.

Iron Deficiency Anaemia:

The normal adult body contains 4000 mg of iron. About 60% of this iron is present in the circulating blood. The remaining is stored in the liver and reticuloendothelial cells of bone marrow.

When iron is being utilized by the RBC at a faster rate and the dietary intake of iron is insufficient to keep up with the increased use, the iron stored in the body is used for the synthesis of haemoglobin. When the iron stores become exhausted, iron deficiency anaemia results.

Microcytosis, hypochromia and poikilocytosis are associated with iron deficiency anaemia. Reticulocyte count is normal, serum iron is decreased. It is commonly seen in early stages of life and during pregnancy.

Pernicious Anaemia:

This disease is caused by vitamin B₁₂ deficiency. Intrinsic factor, which is necessary for the absorption of vitamin B₁₂ is not secreted by the gastric mucosa. This type of anaemia is generally found in patients above age of 60 year. It is associated with weakness and shortness of breath, abdominal pain, diarrhoea, nausea, pale and sore tongue.

The laboratory findings are macrocytic normochromic RBC, moderate to marked anisocytosis and poikilocytosis serum bilirubin may be increased.

Haemolytic Anaemia:

Haemolytic anaemias are characterized by a fall in haemoglobin, jaundice, dark urine, increasing reticulocytosis. It may be hereditary or acquired. Red cells are usually normochromic and microcytic. Serum / plasma appear yellow due to increased bilirubin.

Haemoglobin and haematocrit varies from normal to extremely low levels. Coomb’s test is positive.

Sickle Cell Anaemia:

In this case, the red cells contain 90 to 100% haemoglobin S, and the remaining is Hb F. It is associated with severe abdominal bone and joint pain, enlarged spleen. Sickle cells are found in blood. Reticulocytes and platelets are increased. Osmotic fragility of RBC is decreased.

Sideroblastic Anaemias:

Sideroblastic anaemia may be hereditary or acquired. In case of hereditary sideroblastic anaemia, it may be present at birth or during infancy and usually manifests in adolescence. RBCs are hypochromic and microcytic. Increased serum iron level, moderate anisocytosis and poikilocytosis.

In case of acquired sideroblastic anaemia, normochromic RBCs but very few are hypochromic red cells. It is found in adults above 50 year of age.

Thalassemia (Cooley’s anemia):

It is a hereditary blood disease, widespread in Mediterranean countries, Asia and Africa, in which there is abnormality in the protein part of haemoglobin molecule. The affected red cells cannot function normally, leading to anaemia. Other symptoms include enlargement of the spleen and abnormalities of the bone marrow.

Individuals inheriting the disease from both parents are severely affected. This is called as thalassemia major. Those inheriting from single parent are thalassemia minor. These are usually symptom free. Patient with major disease is treated with repeated blood transfusions. The disease can be detected by prenatal diagnosis including amniocentesis.

Schilling Test:

Schilling test is a test for diagnosing vitamin B₁₂ deficiency. In this test, first give 1 mg unlabelled vitamin B₁₂ parentally, to the patient. Then give 1 mg labelled vit. B₁₂ orally. It is labelled with ⁵⁷Co. within 24 hours. 1/3rd of absorbed labelled/ radioactive vit B₁₂ is flushed out in urine.

Normal excretion is above 10% of oral dose. In anaemic patients with vit. B₁₂ deficiency, patients excrete less that 5%. If the test is normal, no further testing is necessary.

If it is abnormal, repeat the said procedure with simul­taneous oral administration of intrinsic factor, i.e. vitamin B₁₂ binding protein. If excretion increases, it implies lack of intrinsic factor. If it does not, then there is some defect in absorption. The test should be repeated after 48 hours.