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Unit 3 rbc disorders
- 1. Red cells disorders ●Mature red blood cells have no nucleus and have the shape of biconcave disks ● This shape is to increase the amount of membrane available on each cell, this provide the best surface area to transport the oxygen ● Red blood cells are very flexible and can pass through very small capillaries, even capillaries smaller than the red blood cell. This ensure that oxygen can be brought everywhere in the body ● If a red blood cell is less flexible it can be broken when passing through small capillaries
- 3. Anaemia ● Anaemia canbe defined as a decrease in the concentration of haemoglobin below normal for age and sex. It can also be seen as a decrease in the amount of oxygen available to the cells and tissues of the body ● Typically below 13.5g/dl for adult males and below 11.5g/dl for adult females. From the age of 2 years to puberty below 11g/dl ● Low Hb is usually accompanied by low RBC count and low PCV. This can be normal in some patients with low Hb. ● Dehydration can sometime mask anaemia and increase plasma volume can look like anaemia when it is not (in pregnancy).
- 4. The signs ofanaemia: a. Overall condition of the patient: tiredness or weakness, or appears pale b. Gently pull down the lower lid and look if the membranes of the inner eyelid is pale (white to pink) instead of red. c. Use a small torch to examine the top of the tongue, the lips and the gums. They are pale in anaemic patience.
- 5. The signs ofanaemia: d. Without any pressure observe the area under the finger nails for pallor. e. Extending the fingers, observe pallor of the palm of the hand. f. If anaemia is very severe, face and feet may be swollen, the heart beat rapid and the person may have shortness of breath. Pictures from Anemia Detection Methods in Low- Resource Settings: A Manual For Health Workers
- 6. ● Rapidly progressinganaemia causes more symptoms than anaemia progressing very slowly. ● Severity: Mild anaemia can have no or little symptoms. ● Age: Old people have more symptoms than younger people
- 7. The red bloodcells morphology can help us to identify the cause of anaemia The red blood indices (MCH, MCHC,MCV), Reticulocyte count, some chemistry tests or bone marrow examination are also helpful in finding the cause of anaemia, but blood morphology is cheap and easily available. The equipment needed is found in all small laboratories, some slides, a staining rack with Wright stain, a microscope.
- 8. Haemoglobin ● Haemoglobin ismade from 2 pairs of globin chains to each of which is attached one molecule of Heme. ● HbA has 2 α chains and 2 β chains ● HbF has 2 α chains and 2 γ chains ● HbA2 has 2 α chains and 2 δ chains Normal adult haemoglobin composed of 96% HbA, 3% HbA2 and 1% HbF. At birth Fetal haemoglobin F is predominant, but it reach adult distribution between between 6 and 12 months of age.
- 10. Adult human bonemarrow synthesizes 4 X 1014 molecules of hemoglobin every second. Heme is manufactured in mitochondria and globin chains (alpha and beta) in cytoplasm. They are combined in cytoplasm. Four major problems can happen during this delicate process: Qualitative defects of globin chain synthesis result in hemoglobinopathies such as sickle cell disease. Quantitative defects of globin chain synthesis result in hemoglobinopathies such as thalassemia. Defects in synthesis of the heme portion result in porphyrias. Defects involving incorporation of iron into the heme molecule result in sideroblastic anemias.
- 11. Classification of anaemia ●Aetiological classification based on the cause of anaemia. ● Morphological classification based on MCV, MCH, MCHC and blood cell morphology of blood smear.
- 12. Aetiological classification ● Reducedred cell survival due to haemolysis or blood loss ● Defective production of red cells ● Increased pooling of normal cells in a large spleen ● Sequestration of abnormal red blood cells in the spleen or sometime liver (Sickle cells, Hb C disease) ● Other rare abnormalities ● Pancytopenia (all blood cells are low)
- 13. In short ● Problemwith cells production – Nutritional Iron, Vit12, folate, B6 deficiency – Something involve with Hb production – Kidney dysfunction – low erythropoietin (Check urea, creatinine) ● Abnormal destruction of cells (Live spend 120 days) – Haemolytic anaemia – Anaemia of chronic disease (Inflammation) ● Blood loss – Heavy loss during menstrual cycles – GIT bleed – Accident, surgery
- 14. Morphological classification ● Normochromic,normocytic anaemia – RBC number ↓ – Hb ↓ – PCV ↓ – MCV Normal – MCH Normal – MCHC Normal – RDW Normal – Morphology on smear Normal, but blood is thin.
- 15. Cause of Normochromic,normocytic anaemia ● Acute blood loss ● Anemia associated with leukemia ● Aplastic anaemia ● In some abnormal cell production
- 16. Morphological classification ● Hypochromic,microcytic anaemia – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↓ – MCH ↓ – MCHC ↓ or normal – RDW ↑ – Morphology on smear hypochromic, microcytic and often with anisocytosis. Cells appear small and with a big central pallor
- 17. Cause of Hypochromic,microcytic anaemia ● Iron deficiency anaemia ● Thallassaemia ● Lead toxicity ● Hemoglobin E disorder ● Chronic disease
- 18. Morphological classification ● Normochromic,macrocytic anaemia – RBC number ↓↓ – Hb ↓ – PCV ↓ – MCV ↑ – MCH ↑ – MCHC normal – RDW ↑ – Morphology on smear normochromic, macrocytic and often with anisocytosis. Some of the cells are large and with a normal central pallor
- 19. Cause of Normochromic,macrocytic anaemia ● Megaloblastic anaemia due to vit. B12 or folic acid deficiency ● Pernicious anaemia (condition where B12 cannot be absorbed) ● Hypothyroidism (pernicious anaemia occure 20 times more in patients with Hypothyroidism) ● Aplastic anaemia (Mild macrocytosis can occur in aplastic anaemia, especially at recovery time) ● Liver disease
- 20. Morphological classification ● Normochromic,microcytic anaemia – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↓ – MCH ↓ – MCHC normal – RDW ↑ – Morphology on smear normochromic, microcytic and can have anisocytosis. Cells are small and with a normal central pallor
- 21. Cause of Normochromic,microcytic anaemia ● Anaemia associated with chronic infection ● Other chronic diseases
- 22. Iron deficiency anaemia ●Iron deficiency anaemia is the most common cause of anaemia in the world. 500 million people worldwide. ● Normal adult body contain about 4g of Iron. ● Every day 20 to 25 ml of blood are broken down as normal blood cells renewal. When cells dye they release around 25mg of iron, around 19-24mg is used to make new cells and 1mg is excreted in urine, bile, nails, hair and skin. ● 1mg of iron is the minimum daily intake ● Extra iron should be taken during infancy, childhood and pregnancy. ● We have iron storage in Liver, reticuloendothelial cells and bone marrow that is used when diet iron is insufficient ● When iron store are empty, iron deficiency anaemia starts
- 23. ● Heme ismade of porphyrin and iron. If iron is missing heme can’t be produced and anaemia appears ● Ferritin is a protein-iron complex. It is found in liver, spleen, bone marrow and skeletal muscle. Small amount circulate in blood. Serum ferritin is a good indicator of the body iron store. (<12μg/L (or ng/ml)in iron deficiency anaemia) (Normal 40- 340μg/L. Up to 500μg/L in iron overload)
- 24. Cause of Irondeficiency ● Iron nutritional intake is too low for needs (Often during childhood and pregnancy) ● Mal -absorption of iron ● Increase loss of iron (mainly during GIT or Uterine loss) ● Combination of the above factors ● Rarely sequestration of iron
- 25. Iron deficiency anaemiamorphology ● In the beginning Iron deficiency anaemia show normochromic, normocytic anaemia ● Later it becomes hypochromic and microcytic when Hb is below 10-11g/dl ● Poikilocytosis, including ovalocytes, pencil cells and few target cells can be seen ● Polychromasia is sometime present
- 26. Iron deficiency anaemiaautomated full count ● Early sign of Iron deficiency anaemia is a increased RDW (Cell distribution width) – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↓ – MCH ↓ – MCHC ↓ or normal – RDW ↑
- 27. Look at hemosurfRed Blood Cells Blood film 3
- 28. Anaemia of chronicdisease ● Caused by chronic infection or inflammation which attack the phospholipid membrane of the RBCs by oxidative stress. ● At the beginning anaemia is normochronic, normocytic because production is normal, there is no deficiency, Iron B12, folic acid B6 are all available to make normal cells. As it becomes more severe it is hypochromic and microcytic. ● RDW is often reported as normal. Reticulocyte count is low ● Neutropenia, thrombocytosis, rouleaux formation can be present due to chronic inflammation.
- 29. Anaemia of chronicdisease ● Differential diagnosis include iron deficiency anaemia and thalassemia. ● Serum iron and ferritin normal or high, Hb electrophoresis normal. ● Bone marrow Perl’s stain will show ring sideroblasts. ● Also look at tests like CRP and ESR blood test marker for inflammation
- 30. Comparison of laboratorytests Iron deficiency aneamia Anaemia of chronic disease Thalassaemia trait Serum Iron Reduced Reduced Normal Serum transferrin / serum iron binding capacity Increased Decreased Normal Serum ferritin Reduced Increased Normal Bone marrow iron Absent Present Present
- 31. Sideroblastic anaemia ● Bonemarrow produce ringed sideroblasts instead of healthy RBC precursors. Iron is available but cannot be incorporate into haemoglobin. Granules of iron accumulated in the mitochondria surrounding the nucleus. ● It can be either a rare genetic disorder or acquired as part of myelodysplastic syndrome or B6 deficiency.
- 32. Sideroblastic anaemia morphology ●Blood smear can show anisocytosis or uniform hypochromia, microcytosis in congenital form and normocytic or macrocytic cells with only small population of hypochromic microcytic cells in acquired. ● Few target cells and basophilic stippling may be present ● Poikilocytosis is sometime marked
- 33. Sideroblastic anaemia automated fullcount – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↓ – MCH ↓ – MCHC ↓ or normal – RDW ↑ or normal
- 34. Sideroblastic anaemia furthertests ● Serum iron Normal or ↑ ● Ferritin Normal or ↑ ● Haemoglobin electrophoresis Normal ● Bone marrow Perl’s stain shows ring sideroblasts
- 35.
- 36. Megaloblastic anaemia ● Inmegaloblastic anaemia there is an increased size of erythroid precursors and asynchronous maturation of nucleus and cytoplasm. Cytoplasmic maturation is in advance on nuclear maturation ● Megaloblastic anaemia is usually due to vitamin B12 or folic acid deficiency. But it can sometime be due to drugs affecting DNA synthesis ● B12 and folic acid are both necessary for DNA duplication and therefore cells formation.
- 37. Pernicious anaemia ● Perniciousis a megaloblastic anaemia due to malabsorbtion of B12 because of lack of IF ● Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the cells of the stomach. It is necessary for the absorption of vitamin B12 later on in the small intestine. Pernicious anaemia is a autoimmun condition that attack the production of IF
- 38. Megaloblastic anaemia morphology ●Anaemia ● Macrocytosis ● Anisocytosis ● Poikilocytosis (Including oval macrocytes and tear drops) ● Neutrophil hypersegmentation
- 39. Megaloblastic anaemia morphology ●Sometime hypersegmatation of eosinophil, macropolycytes and basophilic stippling can be seen ● As anaemia becomes more severe, there is increased anisocytosis, poikilocytosis with appearance of microcytes and cell fragments. ● Small number of Howell-Jolly bodies and immature cells can appear ● Number of WBC and platelets are falling ● No polychromasia and reticulocyte count is low
- 40. Other Tests ● Microbiologicaltest (use growth of micro- organism to deduce level of B12 ) ● Radioisotope assay ( Schilling test) test in urine the ability to absorb 57 CO labelled B12 orally. ● Microbiological test (use growth of micro- organism to deduce level of folate) ● Radioisotope assay ( cow’s milk as binding protein) test in urine the ability to absorb 57 CO labelled B12 orally. ● Bilirubin (indirect) ↑, Serum iron ↑, ↑LDH with LHD-1 > LDH-2
- 41. Iron, Vit B12and folic acid ● Patient can have more than 1 deficiency. When Iron deficiency is present at the same time than Vit B12 and folate deficiency, there may be hypochromic microcyte at the same time as macrocytes. ● The presence of hypersegmented neutrophils may suggest a double deficiency ● When good treatment is given, WBC, Platelets and RBC increase and we see polychromasia
- 42. Severe anaemia ● Asanaemia become severe, the presence of severe poikilocytosis and cell fragments can decrease the MCV, but the RDW is then very high
- 43. Megaloblastic anaemia automated fullcount – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↑ – MCH ↑ – MCHC normal – RDW ↑ (the increase of RDW precedes the MCV ↑)
- 44. Macrocytic anaemia dueto liver disease ● Alcohol intake and chronic liver disease can cause macrocytic anaemia. ● Morphology shows round macrocytes (not oval), target cells and stomatocytes. ● Sometime neutropenia and throbocytopenia. ● No hypersegmented netrophils ● Hb, RBC and PCV ↓ ● MCV and MCH ↑ ● MCHC Normal ● RDW often normal ● Liver function tests are useful (γGT)
- 45. Look at HemosurfRedBlood Cells Blood film 4
- 46. Blood loss ● Anaemiathrough blood loss can happen in young women because of Heavy menstruation ● In male and menopausal women the main cause of blood loss is GIT bleed ● Acute blood loss can happen in accident and surgery. In Acute blood loss the anaemia is not seen during the first day, as it takes time for the body to replace plasma volume. When anaemia is seen indices are normal. ● With chronic blood loss, indices are also normal in early stages and becomes similar to Iron deficiency in severe stages.
- 47. Blood loss ● Acuteat the beginning ● RBC N ● Hb N ● PCV N ● MCV N ● MCH N ● MCHC N ● RDW N ● Acute after plasma replacement ● RBC ↓ ● Hb ↓ ● PCV ↓ ● MCV N ● MCH N ● MCHC N ● RDW N ● Chronic severe ● RBC ↓ ● Hb ↓ ● PCV ↓ ● MCV ↓ ● MCH ↓ ● MCHC ↓ ● RDW N ● Chronic early ● RBC ↓ ● Hb ↓ ● PCV ↓ ● MCV N ● MCH N ● MCHC N ● RDW N
- 49. Haemolytic anaemias ● Lifeof RBC is about 120 days. Then they are destroyed and haemoglobin is broken down is haem and globin. ● Iron is free and recirculate attached to plasma transferrin to bone marrow to be used to make new RBCs. ● Globin chains are broken down to amino acids and reused to make proteins.
- 50. 1) RBC live120 days, then they are broken down. Hb into heme and globin 2)Heme is degraded into biliverdin by phagocytes 3)Biliverdin is reduced to bilirubin 4)Insoluble bilirubin is bound to albumin to go to hepatocytes 5)In the hepatocyte bilirubin is congugated to glucuronic acid to make it soluble 6)Conjugated bilirubin is excreted into bile and reaches the intestin 7)Conjugated Bilirubin is deconjugated by bacteria in the colon and eliminated in feces as stercobilinogen (10% is reabsorbed in blood and excreted by the kidneys in urine as urobilinogen).
- 51. Haemolytic anaemias ● Haemolyticanaemia results from an increase in the rate of red blood cell destruction. ● Increase products from Hb metabolism ● Bone marrow compensate the loss in producing more RBCs. But anaemia occurs when Red blood cells are destroyed faster than they can be replaced. ● Haemolytic anaemia can be inherited or acquired
- 52. Inherited Haemolytic anaemia ●Red blood cells are prematurely destroyed due to defects passed through genes from parents to child. ● The abnormal genes affect the production of RBCs and these abnormal RBCs are destroyed earlier. ● There are many types of inherited Haemolytic anaemias. Some due to faulty haemoglobin. As the cells is not able to carry oxygen normally the body tend to destroy it.
- 53. Abnormal haemoglobin and Thalassemia ●Normal adult haemoglobin composed of 96% HbA, 3% HbA2 and 1% HbF. At birth Fetal haemoglobin F is predominant, but it reach adult distribution between between 6 and 12 months of age. ● 3 problem can occur: – Alteration in the structure of Hb, as in HbS (Sickle cell) – Can’t make enough of one or more of the globin chains, as in Thalassemia – Fails to switch from foetal HbF to adult HbA, as in Hereditary Persistence of Foetal Hb (HPFH)
- 54. Inherited Haemolytic anaemia ●Haemolytic anaemia can also be due to something wrong with the RBC membrane – Hereditary spherocytosis (Cell membrane is sphere-shaped and not biconcave-shaped) – Hereditary elliptocytosis (oval shape) ● Haemolytic anaemia can also be due to something wrong with the RBC metabolism – Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency. An enzyme is lacking that is protecting cells against toxins. Without this enzyme cells are destroyed when these toxins are present
- 55. Acquired Haemolytic Anaemia ●Red blood cells are prematurely destroyed by factors acting on them as they circulate. – Drug-induced haemolytic anaemia: drugs bind to the surface of the red blood cell and antibodies develop. The cell is destroyed in the spleen. – Autoimmune haemolytic anaemia: the person’s immune system malfunctions and makes antibodies that act against the cells – Transfusion reaction, if the wrong group is given. – Exposure to toxins or infections (Snake venom and maleria) – Mechanical damage: surgery, artificial heart valves, high blood pressure can damage RBC membrane, chemical injury (lead poisoning)
- 56. Lead poisoning ● Poisoningwith Lead affects Haem synthesis and causes haemolysis ● Sign of lead poisoning: – Abdominal pain – Constipation – Lead line on gums ● Lead poisoning is more common in children than in adults.
- 57. Lead poisoning morphology ●Can be hypochromic, microcytic or normochromic normocytic with some polychromasia ● Coarse basophilic stipplings ● Pappenheimer bodies may be present ● Reticulocyte can be increased
- 58. Lead poisoning automatedfull count – RBC number ↓ – Hb ↓ – PCV ↓ – MCV ↓ or normal – MCH ↓ or normal – MCHC ↓ or normal – Serum lead elevated
- 59. Globin abnormality -Sickle cell anaemia (HbS) ● Sickle cell anemia is an autosomal recessive disease that result from an abnormal haemoglobin HbS. (1 amino-acid, glutamic acid is replaced by valine in the beta-chain). ● Sickle cells have low oxygen concentration and break easily, Their lifespan is only 10-20 days. (Crescent like shape) ● People with heterozygous HbS, usually don’t show any symptom, they have a normal life
- 60. Sickle cell anaemia(HbS) ● People with Homozygous HbS have obstruction of small blood vessel causing death of local tissue ● Painful crises affecting fingers and toes (in young children), limbs, abdomen and chest. ● More frequent is people of African descent.
- 61. Sickle cell anaemiamorphology ● Anisocytosis ● Anisochromia ● Sickle cells ● Target cells ● Polychromasia ● Basophilic stipplings ● NRBC ● Reticulocyte count is between 10%-20%
- 63. Globin abnormality –HbC ● Hb C is also due to a exchange of amino-acid in beta-chain. HbC is less soluble than HbA and in sufficient amount tends to form crystals within RBCs. ● HbC also affect mainly people of African descent. They have enlarged spleens without other clinical symptoms.
- 65. Thalassemia ● Thalassemia isan inherited blood disorder characterized by an abnormal production of hemoglobin. ● More risk to people from Mediterranean, African, Middle Eastern and Asian descent
- 66. Thalassemia ● Symptoms of thalassemiamay include: – fatigue – pale skin – jaundice – slower growth in children – Large spleen and liver – Bone deformities ● Defects in alpha or beta chains of the globin part of the haemoglobin. The names of alpha and beta thalassemia come from the different defect on these chains. ● The more the genes are mutated the more severe anaemia will be
- 67. ● Blood disordersthat develop if one or more of the four alpha chain genes are missing or mutated. ● Alpha protein chain production depend on 4 genes, you get 2 from your father and 2 from your mother ● The more genes are missing the more severe the condition is Alpha Thalassemias
- 70. αThalassemia Minor Morphology ●In αThalassemia Minor, we usually have a microcytosis, even if there is no anaemia. ● If there is Hypochromia, there is no anisochromia ● Poikilocytosis is mild
- 71. Haemoglobin H disease ●The lack of 3 α genes causes Hb H disease with more symptom as slpenomegaly and hepatomegaly and bone deformities like in β Thalassemia major. ● Morphology: marked hypochromia, microcytosis, Poikilocytosis with target cells, teardrop cells and cell fragments. Basophilic stipplings and polychromasia.
- 72. Haemoglobin H diseaseautomated full count – Hb ↓ – PCV ↓ – MCV ↓ ↓ – MCH ↓ ↓ – MCHC ↓ – RDW ↑ – Reticulocyte count ↑
- 73. Beta Thalassemias ● Blooddisorders that develop if one or both of the two beta chain genes are mutated or rarely absent. ● When only 1 gene is affected this is called Thalassemia Minor ● When both genes are affected this is called Thalassemia Major or Cooley’s Anaemia, patients show a severe anaemia, hepatomegaly, splenomegaly, expansion of red marrow-containing bones with head bones deformities
- 75. ● The reduceβglobin production results in reduce haemoglobin production HbA. To compensate there is an increase number of RBCs but the are microcytic and hypochromic. ●
- 76. βThalassemia Minor Morphology ●In βThalassemia Minor, we usually have a microcytosis, even if there is no anaemia. ● If there is Hypochromia, there is no anisochromia ● Poikilocytosis goes from mild to marked with target cells. ● Basophilic stippling is common ● Reticulocytes count is often increased
- 77. βThalassemia Minor automatedfull count – Hb N – PCV N – MCV ↓ ↓ – MCH ↓ ↓ – MCHC N – RDW N (When anaemia develops it increases)
- 78. βThalassemia Major Morphology ●In βThalassemia major anaemia is severe sometime as low as 2-3gr/dl ● Blood smear show marked anisocytosis, and poikilocytosis with target cells, tear drops, elliptocytes, cell fragments and many bizarre shapes. ● Basophilic stipplings and Pappenheimer bodies present ● Nucleated RBCs are frequent.
- 79. Further tests ● Haemoglobinelectrophoresis
- 80. Treatment of Thalassemia ●It depends on the severity of symptoms ● If you have a mild form of Thalassemia you might have no symptom and therefore no need for treatment ● Moderate to severe conditions require regular blood transfusions, it can be as often as every few weeks. ● This frequent transfusions can overload the body with iron and accumulate in some organs like the heart or liver. The excess iron needs to be removed by medication. ● Bone marrow transplant would be a cure, but it is very difficult to find the right bone marrow donor and it is risky.
- 81. Myelophthisic anaemia ● Myelophthisicanaemia is a severe kind of anaemia due to bone marrow infiltration either fibrosis, leukaemia and other cancers. The bone marrow totally invaded with cancer cells can not produce normal blood cells. ● Morphology includes – NRBCs – Teardrop-shaped cells (Dacryocytes) – Immature cells (produced outside the bone marrow)
- 82. Polycythemia vera ● Polycythemiavera is a discorder of the bone marrow in which too many Red Blood Cells are being produced. 8 to 9 million/ml sometime up to 11million/ml ● This is rare disorder that happen more in men than in women and over the age of 40. ● WBC (Neutro and Baso) and Platelets can also be increased ● Ht (PCV) can be as high as 70-80% ● Blood is very viscus and capillary can be blocked.
- 83. Blood smear ● Showa “packed film”, because the blood is so viscous the blood cannot be spread as thinly as normal. ● RBCs are normochromic, normocytic, or sometime if the iron has all been used up, microcytic, hypochromic. ● RBC, Hb and Ht high ● MCV and MCH Normal or low ● MCHC and RDW are Normal ● If Iron deficiency MCHC low and RDW high.
- 84. Pseudo- polycythemia ● Wecan have a polycythemia that is caused by plasma decreased ● In the case RBC, Hb and Ht will be increased, but WBC and Plts count will be normal. The blood film appear paked but normal.
- 85. Erythroblastosis fetalis ● Haemolyticanaemia of the foetus or newborn. ● It is due to antibodies from the mother crossing the placenta and attacking the foetus Red Blood Cells. It is often seen in Rhesus negative mothers with Rhesus positive babies. It can also be due to anti-Kell or rarely ABO. ● Morphology shows polychromasia (increased reticulocytes and Normoblasts (NRBC).
- 86. Haemolytic disease ofthe Newborn (HDN)
- 87.
- 88. Aplastic anaemia ● Aplasticanaemia is a rare disease in which the bone marrow doesn’t produce enough blood cells. ● It usually touch all 3 cells types (pancytopenia): RBC →aneamia, WBC → leukopenia, platelets → thrombocytopenia. ● It can be pure red cell aplasia, in that case WBC and Plts are normal.
- 89. Morphology ● Ususally normochromic,normocytic or macrocytic ● Sometime anisocytosis and poikilocytosis
- 90. References ● Barbara J.Bain, Blood Cells, A Practical Guide ● Dacie and Lewis, Practical Haematology ● University of Washington, MTS, Lab Training Library, Peripheral Blood ● Godkar, Textbook of medical laboratory technology ● Hemolytic Anemia and Thalassemia videos, Md.Shariful Islam ● Wikipedia
Editor's Notes
- #3 Glucose enter into a cell, it goes through glycolysis. Glucose which is 6 Carbons is broken down into 2 Pyruvate that are each 3 carbons molecules. This makes 2 ATP. Pyruvate can enter into the mitochondria (power house of the cell). That means that in the mitochondria we are going to make ATP. ATP is need in all cells to run the cell. The more ATP the cell has the better the cell can do its job. If ATP can’t be made this will result in illness. Pyruvate in the mitochondria is converted into Acetyl CoA which goes into the citric acid, in which only 1 ATP is made. The real role of the Acetyl Acid cycle is to produce electrons. They get transferred to the electron transport chain. These electrons are transported down into these proteins and the last protein complexe donate its electron to oxygen. If someone is anaemic and don’t transport enough oxygen to the cells, this last step cannot happen and the electron transport chain cannot produce their normal 32 to 36 ATP
- #11 http://emedicine.medscape.com/article/1389794-overview
- #14 Inflammation: membrane of RBC are made of phospholipids that can be oxydased and destroyed prematurely
- #32 Sideroblasts (sidero- + -blast) are atypical, abnormal nucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in the mitochondria surrounding the nucleus. Normally, sideroblasts are present in the bone marrow, and enter the circulation after maturing into a normal erythrocyte. https://en.wikipedia.org/wiki/Sideroblastic_anemia
- #40 An unusually large polymorphonuclear neutrophilic leukocyte that contains a multisegmented nucleus (8, 10, or more lobes); the arrangement of chromatin is less compact than in the normal neutrophil, and the cytoplasmic granules tend to be larger and more acidophilic. Such changes frequently precede significant alterations in the red blood cells, as in pernicious anemia and certain other forms of anemia. http://www.medilexicon.com/dictionary/52210
- #51 http://www.hepatitis.va.gov/HEPATITIS/course/index.asp?page=/provider/courses/livertests/livertests-13&
- #53 https://www.youtube.com/watch?v=qUSVlKKr1qA
- #57 https://www.medicaljournals.se/acta/content/html/10.2340/00015555-1201
- #60 http://www.slideshare.net/drramnegi/thalassemia-and-hemoglobinopathies
- #69 https://en.wikipedia.org/wiki/Alpha-thalassemia
- #70 http://www.pathwaymedicine.org/alpha-thalassemia
- #81 Show video “All about Thalassemia Cartoon”
- #91 https://www.youtube.com/watch?v=qUSVlKKr1qA