Red and white blood cells

Red blood cells (erythrocytes) are biconcave discs without a nucleus (lack the ability to repair themselves).
Lifespan is approximately ~100–120 days.
The cells are flexible, which makes it easier for them squeeze through the narrow capillaries.
Erythropoiesis – The process of RBC production in marrow. The process is stimulated by Erythropoietin which is produced from the Kidneys in adults [From LIVER in fetal life]. It stimulates the bone marrow.

In renal failure patients, we supplement Erythropoietin / Darbepoetin regularly to avoid anemia as the kidneys have failed.

Clinical pearl

RBCs are produced in the bone marrow of the adult, and liver and spleen of the fetus.

Major stimulus for increased erythropoietin release is low O₂ (hypoxia).

Haemoglobin synthesis requires iron, folate and vitamin B12. Deficiency of any of those will lead to anemia (Low Hb).

• B12 and Folate deficiency – Megaloblastic anemia
• Iron deficiency – Microcytic hypochromic anemia

Reticulocyte – young RBCs that shows a reticulum on staining. A matured RBC will not have retinaculum and it’s biconcave in shape.

Reticulocytosis – Normal circulation may have 1–2% of circulating reticulocytes. But, for some reason if RBC productions is increased, young RBCs might enter the circulation even before they fully mature.
Increased production can occur when hypoxia induces excess erythropoietin production that stimulates the bone marrow to produce more RBCs.

The produced RBCs are stored in the Spleen which will be released as needed.
At the end of life span (~120 days) of if they get damaged, RBCs will be destroyed (Sequestered) by the macrophages in the liver and spleen.
The haem group is broken down to biliverdin and then bilirubin.
Excessive breakdown results in excess bilirubin (Clinically seen as Jaundice).

Sickle cell disease will lead to excessive sequestration of RBCs in spleen.
Splenectomy is indicated in them ( Risk of infections from encapsulated organisms is high post splenectomy)

Clinical pearl

Red cells have surface antigens on them that form the basis of blood groups (A-B-O and Rh).

White blood cells

White blood cells ( also called as leucocytes) play a key role in defense mechanisms in the body to fight the infection. WBCs are produced in excess and counts increase in infection.

Types of Leucocytes

1. Granulocytes
   • Neutrophils
   • Eosinophils
   • Basophils
2. Lymphocytes
   • B cells
   • T cells
   • NK cells
3. Monocytes (–> Macrophages)

Granulocytes

have granules that stain to dyes. Neutrophils have neutral-staining granules, Eosinophils have acid-staining granules and Basophils have basic-staining granules.

Neutrophils reach the site of infection (via chemotaxis) within minutes and start destroying bacteria by phagocytosis.
Neutrophils constitute a major component of pus.

Eosinophils are longer lived. They phagocytose larger parasites.
Their counts increase in allergic disease.

Basophils and mast cells are similar – both release histamine and heparin as inflammatory response.

Neutrophils are the first to accumulate at infection site

Frequently tested

Lymphocytes

Produced in the bone marrow but mature in the lymph nodes, thymus and spleen.
Lymphocytes are critical components of the immune system and are of three main forms:

• B cells – produce γ-globulins (immunoglobulins, antibodies),
• T cells – coordinate the immune response,
• Natural killer (NK) cells – kill infected / cancerous cells.

Monocytes

phagocytic in nature but are larger and longer lived than granulocytes.
After formation in the marrow, reach tissues to become macrophages.

Macrophages

They form the reticuloendothelial system RES in liver, spleen and lymph nodes. Apart from regular phagocytosis, these help clear dead cell debris also.