Blood Disorders|Types of Anaemias

DISORDERS OF THE BLOOD

Anaemia: This is the reduction in the oxygen-carrying capacity of the body, normally as a  result of the reduction in red blood cells. This causes a reduction in hematocrits and a general decrease in haemoglobin levels are seen. This can cause an increase in erythropoiesis and increase in erythroid marrow hyperplasia.    Loss of blood can be acute or chronic, in acute blood loss, if the person survives, the Marrow replaces the RBC for example Trauma or bleeding. Chronic is long-term Anaemia that happens when the Iron levels are depleted. This can happen as a result of GI bleeds. Iron is important because the body needs it to be part of the heme molecule of haemoglobin. If they’re not enough Iron, haemoglobin cannot be made, therefore RBC is not.

Types

Haemolytic Anaemias:

This anaemia is caused by the destruction of the RBC prematurely,  can cause a build-up of the broken down products from RBC destruction.  This causes an increase in erythropoiesis and an increase in reticulocyte numbers. The clinical symptoms of anaemia vary but can range from headaches to lack of concentration, palpitation, angina, and shortness of breath. Different types of anaemias are classified in terms of there capsular volumes which is related to red blood cells. Intravascular hemolysis happens within the vascular system by mechanical damage, for example, complement-mediated lysis. Extravascular hemolysis – by mononuclear phagocytosis, particularly in the spleen, happens when there is damage to the RBC membranes which leads to deformity of RBC.

Hereditary Spherocytosis,

This is an autosomal dominant disorder, results in membrane defects or reduction in protein that codes for spectrin. RBCs become spherical, less deformable and are more prone to destruction in the spleen. The cells lose their membranes spontaneously which results in them becoming spherical. They appear as small cells with small central areas missing when the cells are stained. Symptoms of the condition include fatigue, shortness of breath,  irritability, increased heart rate and palpitation to name a few. symptoms include fatigue, shortness of breath, increased heart rate, heart palpitation to name a few.

Sickle cell Disease –

Sickle_cell_01 (1)

This is a hereditary disease due to point mutation, the RBCs appear sickle-shaped. This results in the chronic haemolytic state. The cell membrane is rigid and non-deformable. Results in the sickle cells being destroyed in the spleen. the average survive days of the sickle cells is 20 days, normal RBC lifespan is 115 days.   Microvascular occlusions also happen because the membrane is not elastic which increases the chances of the RBC’s adherence to the endothelium of the capillaries which then cause blockage of the small vessels.

The severity of symptoms will vary from person to person, the Sickle cell can lead to various serious acute and chronic condition. For example Haemolytic crisis where there is an accelerated drop in the levels of haemoglobin, this is particularly common in people with coexisting G6PD deficiency. G6PD is an enzyme designed to produce reduced glutathione in the RBC  monophosphate hexose pathway. Glutathione aids in the prevention of oxidative damage to the haemoglobin and other intracellular structures. Sickle cells anaemia is most common in black people. In America 1 in every 13 black people has sickle cell disease.

Reduced production of RBC

you can also get anaemias from the reduced production of RBC ( erythropoiesis) these kinds of anaemia result from the deficiency in substrates necessary for RBC production. for example Megaloblastic Anaemia– this results from deficiency in B12 or folate, abnormally large RBC precursor cells. Erythropoiesis is not effective, the megaloblasts die in the marrow. You can also have Megaloblast hyperplasia where large oval RBC are produced.  B12 and folate are coenzymes for DNA synthesis, RNA is not affected so the cytoplasm is normal. But the nucleus does not mature, so the anaemia is caused by both ineffective RBC production and the formation of abnormal RBCs.

Pernicious Anemia

Due to lack of intrinsic factor that is normally produced by the parietal cells in the stomach, intrinsic factor is important for the bodies synthesis of B12. Lack of Intrinsic factors is probably due to the autoimmune response to parietal cells.

Aplastic Anemias 

As a result of the suppression of the multipotent myeloid cells which causes neutropenia, thrombocytopenia, and Anaemia, may also be idiopathic or caused by myelotoxic drugs chemicals that damage the marrow.   Idiopathic can be caused by a defect in the numbers of the stem cells and the functions of the stem cells. It can be cured by bone marrow transplant and suppression of T cell-mediated immune mechanism. This can lead to disorders of platelets, leukocytes, and erythrocytes.

Iron deficiency Anaemias

  • Maybe due to low iron intake, malabsorption, increased demand or chronic blood loss, hyperplasia of the marrow occurs
  • depletion of iron-containing enzymes happen, and in among others, alopecia and atrophy of the mucosa of the Gi tract and the tongue

There a lot more blood disorders we could have covered, the conditions that have covered on are only an overview. These are the notes I used to study for my biology exam. This paper should not be used as a diagnostic tool, if you suspect any of these diseases, see your doctor.

References

Hanna, J., Wernig, M., Markoulaki, S., Sun, C.-W., Meissner, A., Cassady, J. P., . . . Jaenisch, R. (2007). Treatment of Sickle Cell Anemia Mouse Model with iPS Cells Generated from Autologous Skin. Science, 318(5858), 1920-1923. doi:10.1126/science.1152092

Fitzsimons, E. J., & Brock, J. H. (2001). The anaemia of chronic disease: Remains hard to distinguish from iron deficiency anaemia in some cases. BMJ: British Medical Journal322(7290), 811.

Beutler, E., & West, C. (2005). Hematologic differences between African-Americans and whites: the roles of iron deficiency and α-thalassemia on haemoglobin levels and mean corpuscular volume. Blood106(2), 740–745. http://doi.org/10.1182/blood-2005-02-0713

Disclaimer; This is purly educational and should not be used as diagnostic tool, if you suspect any these, seek medical help. 
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