Anemia: Symptoms, Causes, Diagnosis, and Treatment

Anemia may be outlined as the diminished level of Hb% in the blood below the reference level for the age and sex of the individual.

Classification of anemia:

(A) Blood loss Anemia:
1) Acute posthemorrhagic anemia:

  • Trauma, surgery.

2) Chronic hemorrhagic anemia:

  • Peptic Ulcer, Parasitic (hookworm) infestation, Malignancy Bleeding disorder.

B) Increase the rate of destruction of RBCs:
Hemolytic anemia

C) Impaired red cell production:
1) Disturbance of proliferation and differentiation of stem cells.

  • Aplastic Anemia
  • Pure red blood cell aplasia
  • Anemia due to renal failure
  • Anemia due to endocrine disorders.

2) Disturbance of proliferation and maturation of RBCs.
i) Defective DNA synthesis.
Deficiency or an impaired utilization of Vitamin B₁₂ and folic acid.
ii) Defective Hb synthesis.
Deficient heme synthesis.
(Iron deficiency anemia)
Deficient globin synthesis
iii) The abnormal form of Hb:

  • Sickle cell anemia

Classification of Anemia

Blood Loss

  1. Acute 
  2. Chronic

Impaired Production (Hypo-proliferative)

Iron deficiency
Megaloblastic (nuclear-cytoplasmic dyssynchrony):

  • Vitamin B₁₂ or folic acid

Anemia or Chronic disease
Aplastic Anemia congenital or acquired

Increase Destruction (Hemolytic)

Extrinsic to red blood cell:
  • Auto-immune or iso-immune infections
  • Physical or chemical agents

Intrinsic to red blood cell:

  • Membrane defects
  • Enzyme deficiencies (metabolic)
  • Hemoglobinopathies: chain synthesis defects, amino acid substitutions.

Aplastic Anemia:

In this type of anemia, the RBCs, WBCs, and platelets count are decreased due to bone marrow aplasia (defective) or the lack of functioning of bone marrow.

Causes of Aplastic Anemia:

1) Congenital: Fanconi’s anemia.
2) Acquired: Secondary aplastic anemia.
3) Radiation: Hazards of atomic energy and x-rays etc.
4) Chemicals: Benzine and related compounds.
5) Drugs: Chloramphenicol, Sulfonamide, Phenylbutazone, Chlorpheniramine, Chlorpromazine, Carbimazole, Methotrexate, Gold, etc.
6) Miscellaneous: Pregnancy, Tuberculosis, low socioeconomic, and educational reputation or status.

Clinical features:

Clinically a patient has progressive anemia due to decreased RBCs count, hemorrhagic spots in the skin and mucus membrane include bleeding from gums and epistaxis (bleeding from the nose) due to thrombocytopenia and fever with ulcers in the oral cavity and throat are seen due to granulocytopenia.


This type of anemia is treated by bone marrow transplantation, regular red cell concentration transfusion, platelet transfusion, and the use of antibiotics and steroids.

Megaloblastic Anemia

In this type of anemia, the erythroblasts are large, odd-shaped thus the name is megaloblastic anemia. There are two principal types of megaloblastic, one is caused by the deficiency of vitamin B₁₂ and the other is caused by a lack of folic acid.

Causes of Megaloblastic Anemia:

➤Vit. B₁₂ deficiency anemia:

1) Causes of vitamin B₁₂ deficiency:
  • Inadequate intake of diet.
  • Impaired absorption.
2) Intrinsic factor deficiency:
  • Pernicious anemia. 
  • Gastrectomy (surgical removal of entire or part of the stomach).
  • Congenital absence of inherent or intrinsic factor.

3) Disorder of the terminal ileum:

Tropical sprue (malabsorption disease), nontropical sprue, regional enteritis, intestinal resection, neoplasm, and granulomatous disorders.

4) Competition for vitamin B12:
  • Fish type worm infestation.
  • Bacterial blind loop syndrome.

Vitamin B₁₂:

Vitamin B₁₂ is essential for metabolism, the formation of red blood cells, and the maintenance of the central nervous system, which includes the brain and spinal cord.

➤ Folic acid deficiency Anemia:

i.  Inadequate intake of the diet:
  • Unbalanced diet
  • Excessive cooking
  • Common in alcoholics, teenagers, and sometimes in infants.
  • Old age, poor conditions, starvation.

ii. Malabsorption:

  • Tropical sprue
  • Drugs (barbiturates, ethanol diphenylhydantoin).

iii. Increased requirements:

  • Pregnancy, lactation, infancy, malignancy, increased hematopoiesis.

➤ Other causes:

A drug which impairs DNA metabolism:
  • Mercaptopurine
  • Fluorouracil
  • Cytosine

Pernicious Anemia

This is the type of megaloblastic anemia due to the shortage of folic acid.  

Causes of Pernicious Anemia:

Same as causes of megaloblastic anemia.

Clinical features:

A patient with a folic acid deficiency may be asymptomatic, if the deficiency of folic acid is severed, he may present a complex clinical picture, since the malnutrition that is responsible for folic acid deficiency and also produces other deficiencies as well. It most cases the patient may appear obviously malnourished. The onset of the anemia is associated with non-specific symptoms such as weakness, weight loss, easy fatigue, some patient also give a history of lack of concentration, and insomnia. The patient also mentions the symptoms referable to the gastrointestinal tract. These include sore tongue and cheilosis/cheilitis (a disorder of the lips marked by scaling and fissures at the corners of the mouth). But remember this in contrast to vitamin B₁₂ deficiencies, neurological abnormalities do not occur.


This anemia is treated by giving a daily dose of 5mg of folic acid orally. Prophylactic folic acid is also advisable in pregnancy and in persistent hematological disorders, where there is rapid cell turnover. But remember this folic acid never be given other than with vitamin B₁₂ between of risk of aggravating neurological features of vitamin B₁₂ depletion.

Iron Deficiency anemia

This is the type of anemia it occurs when there is an inadequate amount of iron is present for hemoglobin synthesis.

Causes of Iron Deficiency anemia:

Nutritional deficiency:

1. Low intake
2. Increase in demand

  • Pregnancy
  • Infancy
  • Lactation 
  • Excess menstrual flow.


  • Partial/complete gastrectomy
  • Achlorhydria
  • Steatorrhoea
  • Celiac disease
  • Intestinal tuberculosis

Acute/chronic blood loss:

  • Peptic ulcers
  •  Coloniccarcinoma
  • Hemorrhoids
  • Hookworm infections
  • Bleeding disorders

Clinical features:

The symptoms of iron deficiency anemia are similar to all other anemia’s include fatigue, weakness, pallor complexion. Symptoms specific to iron deficiency anemia may include the epithelial changes, brittle nails and hairs, koilonychia (spoon-shaped nail), atrophy of the tongue, glossitis (inflammation of the tongue) and angular stomatitis, dysphagia (difficulty or discomfort in swallowing, as a symptom of the disease).


The correct line of treatment of iron deficiency anemia is to find and treat the underlying cause. Oral iron is advised in the form of ferrous sulfate in the dose of 600mg daily.
If the patient is intolerant of oral preparations due to Plummer Vinson’s syndrome, he may be advised parenteral iron.
Iron dextran can be given in doses of 50-250mg daily by deep intramuscular injections. It is better to give blood transfusion in a case when the Hb is less than 5mg%.

Hemolytic Anemia:

Hemolytic Anemia means (Break down of Red Blood Cells). In this type of anemia, there is early rupturing of the red blood cells and the release of hemoglobin. Different abnormalities of RBCs many of which are hereditary or acquired, make the cells very fragile so that they rupture easily. Even though the number of RBCs formed is completely normal. Their life is so short that it causes anemia.

Causes of hemolytic anemia:

Intracorpuscular abnormalities:

  • Hereditary spherocytosis (RBCs are sphere-shaped).
  • Sickle cell anemia.
  • Thalassemia.

Extra corpuscular abnormalities:

  • Erythroblastosis details.
  • Autoimmune hemolytic anemia.
  • Acquired hemolytic anemia due to toxins bacteria and physical agents.
  • Malaria.
  • Glucose 6 phosphate dehydrogenase deficiency.


  • Drugs damaging to RBCs, hypersplenism.

Hereditary Spherocytosis:

This is an inherited familial disorder that causes a metabolic defect in the RBCs membrane. This leads to increased permeability of the cell membrane to Na+ (which is pimped out). This results in RBCs which are very small in size and spherical in shape, rather than biconcave discs. These cells cannot be compressed because they do not have normal, instead of a loose bag like cell membranes which can easily rupture on even a slight compression.

Clinical features:

The patient suffers from anemia and intermittent attacks of jaundice. The patient is more liable to develop gall stones and ulcers on the legs are quite common.

Hereditary spherocytosis

  • Inherited, intrinsic, membrane defect
  • RBCs – spheroidal, less deformable, and vulnerable to splenic destruction
  • AD – 75%
  • Rest autosomal recessive form
  • Highest incidence in Northern Europe
  • 1 in 5000
  • Lifespan of RBC > 10-20 days


  1. Folic acid 5 mg/day
  2. Blood transfusion
  3. Splenectomy is advisable in all the mild cases

Sickle Cell Anemia

In this type of anemia, there is an abnormal form of Hb called Hb-S which is caused by an inherited genetic defect.

Clinical features:

  • Painful swelling of the hands and feet.
  • Chest pain.
  • Fatigue and intolerance to exercise due to reduced Hb.
  • Pallor, icterus, and splenomegaly.
  • Haematuria (blood in urine).
  • Development of immunity for plasmodium falciparum.


  • Sickling of normoblasts due to low oxygen tension.
  • Hb is less than 8 gm% 
  • The presence of HbS is demonstrated by the examination of RBCs.


  • Sickle cell anemia is treated with folic acid and the infection is treated with antibiotics.
  • Blood transfusion is advised when Hb is falling to 5 gm%.

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