The decrease in RBC count or low haemoglobin in blood is called anaemia. It is because of blood loss due to severe injury or destruction of RBCs or due to less formation of blood. It decreases the oxygen-carrying capacity of the blood.
The symptoms of anaemia are fatigue, weakness, pale or yellowish skin, irregular heartbeats, shortness of breath, headaches, dizziness, lightheadedness, chest pain, cold hands and feet.
Treatment of iron deficiency anaemia usually involves taking iron supplements and making changes in diet.
Polycythemia is a blood cancer caused by a gene mutation. In this diseases, the bone marrow makes too many red blood cells. This causes the blood to thicken and flow more slowly, putting the person suffering from the diseases at the risk of blood clots which can lead to heart attacks or strokes. Polycythemia is treated by phlebotomy (controlled bloodletting) and hydroxyurea (Hydrea).
The decrease in RBC count is called erythrocytoponia. Erythrocytopenia (or erythropenia) literally means the low count of RBCs (red blood cells, erythrocytes) while anaemia may mean low haemoglobin and/or low RBC count.
Erythrocytoponia causes oxygen shortage in blood and tissues. Oxygen shortage stimulates kidneys to secrete hormone erythropoietin into the blood. It stimulates the bone marrow to increase production of RBCs.
It is usually treated with frequent blood transfusions.
This disorder is caused by genetic mutations that prevent the normal production of haemoglobin. When red blood cells do not have enough haemoglobin, oxygen doesn’t get to all parts of the body. Organs then do not function properly. These disorders can result in bone deformities, enlarged spleen, heart problems, retarded growth and development in children.
It is usually treated with frequent blood transfusions. It is also treated with stem cell transplant.
Sickle Cell Anaemia:
Normal red blood cells are smooth and flexible circular discs, enabling them to squeeze and bend to move easily through blood vessels. While, sickle cells are C shaped, stiff, sticky. Sickle cells tend to cluster together and making it difficult for them to move through small blood vessels. These clusters can create blockages in the blood vessels, stopping the movement of healthy, oxygen-carrying blood. This blockage decreases oxygen delivery to the tissues, which can cause pain, organ dysfunction.
It is usually treated with frequent blood transfusions.
The Fate of the RBC’s:
Due to the lack of nuclei and organelles, the mature red blood cells do not contain DNA and cannot synthesize any RNA, and consequently, they cannot divide or repair themselves, limiting their lifespan.
The erythrocytes have no nucleus, no endoplasmic reticulum, and no mitochondria. But there is some glucose oxidation (by glycolysis) which can produce ATP. This ATP is required for flexibility of the cell, membrane ion transport and to keep Fe in the ferrous format for carrying oxygen. The quantity of ATP produced in RBCs is sufficient to keep the RBC membrane flexible for about 120 days.
All RBC’s (of size 7 micron) will at one moment or another flow through the spleen. The capillaries in the spleen are the narrowest and has size of 3 microns. If the RBC is flexible it squeezes through these narrower capillaries. If RBCs are old and nearing the lifespan 120 days are no longer flexible enough, they break during passage through capillaries of the spleen and the breakdown of RBCs takes place.
In the spleen, the components of the old destroyed RBC’s are recycled. Iron Fe is converted into transferrin and then further to Ferrin. Thus iron is recycled. The protein globin is converted back into its amino acids. These amino acids are used for building other proteins. In the spleen, the heme is converted, first into biliverdin which is then converted into bilirubin. This bilirubin is then transported by the blood to the liver. Then bilirubin is secreted into the bile.
The bile is secreted into the intestine, where the intestinal bacteria convert the bilirubin into urobilinogen. This urobilinogen is absorbed by the blood and is taken back to the liver or excreted by the kidney (as urobilin) or excreted via the stool (as stercobilin).
The stercobilin in stool gives the stool its characteristic brown colour. In absence of stercobilin, the stool becomes pale. This change in stool colour is a diagnostic factor that malfunctioning of the gallbladder or the bile duct.
Old young athletes of Grece used to remove spleen to have more RBCs in the blood circulation, to increase the oxygen-carrying capacity of the blood. The RBC’s to die not in the spleen but elsewhere, in the capillaries of the brain, the heart or in the muscles. Due to this, the quality of these organs used to deteriorate and they used to die early.
When someone turns “yellow”, that means that something is wrong with the bilirubin processing.
In this disease too much RBC’s are being destroyed which increases the “free” bilirubin. This can be due to poisoning, a defect in the RBCs, mismatched transfusion etc.
Anaemia-induced jaundice may be treated by boosting the amount of iron in the blood by taking iron supplements or eating more iron-rich foods.
When the liver cells are diseased (such as in hepatitis), then they will be less able to conjugate the bilirubin. This will also increase the “indirect” bilirubin.
Hepatitis-induced jaundice is treated with antiviral or steroid medications.
This occurs when the bile in the liver does not reach the intestine due to obstruction of the bile ducts (gallstones!) or to cholestasis (no bile flow). This will lead to an increase in the conjugated bilirubin.
Doctors can treat obstruction-induced jaundice by surgically removing the obstruction.
If jaundice has been caused by the use of a medication, treatment for involves changing to an alternative medication.