Haemopoietic and lymphoreticular system

10 Haemopoietic and lymphoreticular system


Haemopoiesis is the production of blood cells. In the fetus, blood is formed in the bone marrow, spleen and liver. At birth the marrow is the main site of haemopoiesis, but eventually the red marrow of the long bones is replaced by fat such that, in the adult, red marrow remains only in the axial skeleton, ribs and skull, and in the proximal ends of the humerus and femur.


Erythrocytes are non-nucleated blood cells which are biconcave and deformable. They are the most abundant blood cell and form 45% of the total blood volume, i.e. the haematocrit or packed-cell volume (PCV). Their function is to carry oxygen. About 1% of red cells stain purplish because of residual RNA. They are called reticulocytes. The proportion of these cells in the blood stream increases when bone marrow production of erythrocytes increases, e.g. after haemorrhage. Production of red cells in the bone marrow requires mitosis and maturation, the cells being derived from a pluripotent stem cell. The earliest red cell precursor is the proerythroblast, a large nucleated cell. By a series of divisions, the proerythroblast develops into a non-nucleated cell containing haemoglobin, i.e. an erythrocyte. At the stage of extrusion of the nucleus a reticulocyte is formed which contains remnants of RNA and ribosomes and continues to make haemo-globin. Reticulocytes mature for one or two days in the marrow before being released into the blood where, after a further one or two days, they lose their remaining ribosomes and become mature erythrocytes. Mature erythrocytes survive for 18–120 days in the circulation before being removed by macrophages in the spleen, and to a lesser extent in the bone marrow and liver. Within the macrophage the erythrocyte is broken down into haem and globin. The amino acids of the latter enter the general amino acid pool of the body, while the haem group is broken down with the release of iron which attaches to transferrin. Transferrin is an iron-binding beta-globulin responsible for iron transport and delivery to receptors on erythroblasts, or to iron stores. The remainder of the haem group is converted to bilirubin. Renal secretion of erythropoietin stimulates red cell production to keep pace with the rate of destruction. Erythropoietin is secreted by the kidneys in response to local hypoxia and acts on red marrow, causing an increased output of erythrocytes until the rise in haemoglobin concentration in the blood restores normal delivery of oxygen to the tissues. Erythropoiesis requires an adequate dietary intake of iron, vitamin B12 and folate. Depletion of stores of these will reduce erythropoiesis.


Anaemia is the reduction of the concentration of haemoglobin in the circulation below the normal range. There are three main causes of anaemia: blood loss, haemolysis, and impairment of red cell formation/function.


Haemolytic anaemias are a group of diseases in which red cell life span is reduced. Haemolysis is usually associated with increased erythropoiesis. Laboratory evidence of increased red cell destruction is demonstrated by: (i) increased serum unconjugated bilirubin; (ii) reduced serum haptoglobin; (iii) morphological evidence of red cell damage, e.g. spherocytes, red cell fragments, or sickled cells; (iv) reduced lifespan of red cells, e.g. demonstrated by tagging with radioactive chromium. Laboratory evidence of increased erythropoiesis depends on demonstrating a reticulocytosis in the peripheral blood and erythroid hyperplasia in the bone marrow.

Sickle cell anaemia

This is due to the presence of a haemoglobin variant, HbS, in the red cells. Recurrent painful crises and chronic haemolytic anaemia occur relating to sickling of red cells on deoxygenation. Deoxygenated HbS is 50 times less soluble than deoxygenated HbA and polymerises on deoxygenation into long fibres which deform the red cell into the typical sickle shape. The presence of HbS is the result of a defect in the gene coding for glutamic acid, the latter being replaced by valine. When an individual is heterozygous for this defect, both HbA and HbS are formed, and they are individually said to have sickle cell trait. These individuals are usually haematologically normal and are usually asymptomatic. When only the trait is present the red cells do not usually sickle until the oxygen saturation falls below 40%, which is rarely reached in venous blood. In surgical practice the anaesthetist needs to be aware of the trait so that hypoxia is avoided intraoperatively. When the individual is homozygous, HbA is not formed. The red cells readily deform and sickle cell anaemia develops. Cells sickle at the oxygen tension normally found in venous blood. The increased rigidity of the cells causes them to plug small blood vessels, with resulting infarction and painful crises. Patients may develop acute abdominal and chest pain that mimics other intra-abdominal and thoracic catastrophes. Bone pain may occur and also the patient may develop priapism. The anaemic patient responds poorly to infection, and septicaemia and osteomyelitis may develop, the latter being attributable on occasions to Salmonella. The spleen may calcify and atrophy due to repeated infarction. Pigment gall stones may occur.


White blood cells form part of the body’s defence mechanism. They are divided into two main groups: phagocytes, which engulf and destroy bacteria and foreign matter, and lymphocytes, which are responsible for the immune response. Granulocytes and monocytes develop in red bone marrow from a common stem cell. The granulocyte precursor is a myeloblast which subsequently differentiates and matures, acquiring characteristic granules, to become either a neutrophil, basophil, or eosinophil granulocyte. Precursors do not normally circulate but may do so in case of bone marrow disease or severe infections.

Changes in white cells in disease


Haemostasis is the physiological process by which bleeding is controlled. It consists of four components: vasoconstriction, platelet activation, the coagulation mechanism and the fibrinolytic system.

Fibrinolytic system

During the repair process in blood vessels and healing wounds, fibrin is removed by the fibrinolytic system (Fig. 10.2). Fibrin is broken down to soluble fibrin degradation products by plasmin. Plasmin is derived from the inactive precursor plasminogen by the action of plasminogen activators. Tissue plasminogen activator is released from endothelial cells. Control of the activation of plasminogen is provided by plasminogenactivator inhibitor I, which is released by endothelial cells and rapidly inactivates tissue plasminogen activator.

Dec 12, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Haemopoietic and lymphoreticular system

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