Decrease in the amount of Red blood cells (RBC)/haemoglobin in the blood
Haemoglobin
Oxygen carrying molecule in blood
Full blood count
Essential screening test to investigate suspected anaemia
MCV (Mean Corpuscular Volume)
First step to look at in a full blood count
Full blood counts are commonly requested as part of a general screen in a patient who is unwell to screen for a variety of disorders – such as anaemia, infection, inflammation, nutritional status and bleeding
A blood sample is taken from a vein in the arm or a finger-prick or heel prick (newborns) to perform a full blood count
Haemoglobin
Four subunits, two alpha and two beta, with iron and haem to bind 4 x O2
Normal erythropoiesis
1. Pluripotent stem cell
2. Erythroid burst forming unit (EPO target)
3. Erythroid colony forming unit
4. Erythroblast
5. Reticulocyte
6. Erythrocyte
Underlying causes of anaemia
RBC Loss without RBC destruction (Haemorrhage)
Deficient RBC production
Increased RBC destruction – Haemolytic Anaemias
Haemorrhage
RBC loss without RBC destruction due to trauma, disorders, menstrual flow, gynecological disorders, pregnancy, parasitism
100mls blood = 40 days Fe intake, in a western diet
Regulation of Erythropoiesis
Kidneys monitor blood oxygen, if renal tissue is hypoxic, Erythropoietin is produced by renal peritubular interstitial cells
Factors necessary for erythropoiesis
Erythropoietin
Iron
Vitamin B12 (cyanocobalamin)
Folic Acid (folate)
Ascorbic acid (Vitamin C)
Pyridoxine (Vitamin B6)
Amino acids
Recombinant Erythropoietin (RhuEPO)
Used to treat anaemia in Chronic Kidney Disease, AIDS, Transplant, Cancer, Premature children
EPO is abused by professional cyclists, causes increased blood viscosity, increases Blood pressure, increased heart workload, can lead to heart failure
Haematocrit
Percentage of red blood cells in the blood
Iron deficiency anaemia
Most common cause of anaemia, results in microcytic hypochromic anaemia
Common Causes of Iron Deficiency anaemia
Lack of Iron in diet
Partial gastrectomy due to ulcers
Blood loss due to bleeding peptic ulcers, malignancy
Malabsorption syndromes like Cystic fibrosis, Coeliac Disease
Iron Absorption
Absorbed from the duodenum and upper jejunum, Vitamin C increases absorption by reducing dietary ferric (Fe3+) to ferrous (Fe2+) iron, Caffeine and other xanthines decrease absorption
Normal iron levels are 12g/dL of blood, takes 40 days to obtain Iron in 100mls blood, Therapy is Ferrous Sulfate 200mg 3 times a day, will take 1-2 weeks to raise by 1g/dL
Side effects of oral iron preparations
Nausea
Gastric discomfort
Constipation
Diarrhoea
Darkened stools
Sideroblastic anaemias
A group of conditions diagnosed by finding ring sideroblasts in the bone marrow, both Hereditary (rare) and acquired forms, main defect is reduced activity of enzyme 5-aminolevulinate synthase (ALAS) involved in haem synthesis
Causes of acquired sideroblastic anaemia
Associated with other disorders like Myelodysplastic syndromes, Myeloid leukaemia, Myeloma, Collagen disease
Drugs and toxins like Alcohol, Isoniazid, Chloramphenicol, Lead poisoning
Treatment of sideroblastic anaemia
Main medication is Pyridoxine, if reversible remove offending agent, severe cases require Blood transfusions with iron chelating agent like desferrioxamine
Megaloblastic (macrocytic) anaemia
Due to lack of folic acid or vitamin B12, lack of either prevents formation of DNA so RBC production does not occur or occurs abnormally, results in macrocytic cells (large cells)
Rings
Also known as ring sideroblasts
Causes of acquired sideroblastic anaemia
Associated with other disorders
Myelodysplastic syndromes
Myeloid leukaemia
Myeloma
Collagen disease
Drugs and toxins
Alcohol (e.g. the metabolite acetaldehyde lowers levels of ALAS and pyridoxal)
Isoniazid
Chloramphenicol
Lead poisoning
Treatment of sideroblastic anaemia
1. Main medication - Pyridoxine (may take months to see the benefit)
2. If reversible (e.g. drugs and toxins) - remove the offending agent
3. Severe cases - Blood transfusions (However there is a problem with iron overload - so a chelating agent - e.g. desferrioxamine is required)
Megaloblastic (macrocytic) anaemia
Due to lack of folic acid or vitamin B12
Folate (folic acid) interacts with vitamin B12 and is essential for normal blood and nerve function
Lack of either folate or vitamin B12 prevents formation of DNA so RBC production does not occur or occurs abnormally
Macrocytic cells
Large cells which may have enough Hb, but are not concave and are fewer in number
Cannot take up or transport oxygen normally
More easily damaged - also contributing to the anaemia
Pernicious anaemia
Lack of vitamin B12
Vitamin B12 absorption
1. Must combine with intrinsic factor IF produced by the parietal glands of the stomach
2. The combination enables binding to receptor and phagocytosis of the complex by the distal ileum cells
Pernicious anaemia is usually a result of an autoimmune disease that destroys the parietal cells of the stomach
Vitamin B12
Must be ingested - is not synthesized in body
Sources of vitamin B12
Meat
Eggs
Dairy products
Vitamin B12 can also be administered by injection in pernicious anaemia as cyanocobalamin
Groups at risk of dietary vitamin B12 deficiency
Elderly
Vegans
Alcoholics
Vitamin B12 treatment
1. In normal patients - orally
2. In pernicious anaemia - vitamin B12 can be given via intramuscular injection or parenterally (IV)