Downloaded 60 times
![CLINICAL FEATURES
brittle hair, nail changes
[koilonychia (spoon-shaped)]
dysphagia
(e.g. oesophageal web, Plummer-Vinson ring)
pallor - conjunctiva, palmar creases
glossitis
angular stomatitis
(inflammation & fissuring at mouth corners)
pica
(appetite for non-food substances: ice, paint, dirt)](https://image.slidesharecdn.com/anaemias-bydrdele-180314181253/85/ANAEMIAS-by-Dr-DELE-48-320.jpg)
More Related Content
Similar to ANAEMIAS by Dr DELE
More from Kemi Dele-Ijagbulu
![Hypothalamus short ppt by Dr. Neha [PT].pptx](https://cdn.slidesharecdn.com/ss_thumbnails/hypothalamusbydr-260124145759-b9f94a93-thumbnail.jpg?width=640&height=640&fit=bounds)
ANAEMIAS by Dr DELE
- 1. anaemias by DRKD DELE DEPT. FAMILY MEDICINE DORA NGINZA HOSPITAL
- 2. ANAEMIA: “LACK OF BLOOD” Reduced concentrationof haemoglobin in the blood. The number of red blood cells in the blood is low. If left untreated, can have many serious implications
- 3. DEFINITION A decrease inred blood cell (RBC) mass that can be detected by haemoglobin (Hb) concentration, haematocrit (Hct), and RBC count • adult males: Hb <13.5 gldL or Hct <41% • adult femalc:s: Hb <12 gldL or Hct <36% The World Health Organization (WHO) defines anaemia as hemoglobin concentration <12 g/dL in women and <13 g/dL in men)
- 5. EPIDEMIOLOGY Globally, anaemia isprevalent in most developing countries and of public health significance The global prevalence of anaemia for the general population is 24.8% Women and young children are most vulnerable to anaemia. The proportion of women and children is highest in the Africa region where: 57% of pregnant women, 48% of non-pregnant women, and 68% of preschool children are anaemic Anaemia is also a common, multifactorial condition among older adults.
- 6. EPIDEMIOLOGY, CONT. Anaemia isassociated with poorer survival in older adults More than 10% of community-dwelling adults age 65 years and older are anaemic After age 50 years, prevalence of anaemia increases with advancing age In nursing homes, anaemia is present in 48–63% of residents. Among older adults with anaemia, approximately: one-third have evidence of iron, folate, and/or vitamin B12 deficiency, another third have renal insufficiency and/or chronic inflammation, and the remaining third have anaemia that is unexplained.
- 7.
- 8.
- 9. PATHOPHYSIOLOGY Erythropoietin – whichis produced by peritubular capillary lining cells of the kidney – is critical to the production of red blood cells. Endogenously produced erythropoietin circulates in the plasma to act on specific target cells in the marrow through cell surface receptors. When the oxygen content of body tissues is low or the number of red blood cells decreases, the kidneys produce and release erythropoietin, which stimulates the bone marrow to produce more red blood cells. Iron is bound to the iron transport protein transferrin, and the complex is internalized, along with the transferrin receptor, by the developing erythroid cell. Within the cell, the iron molecule is subsequently split off and either used for haemoglobin synthesis or stored within the cytoplasm as ferritin.
- 10. REGULATION OF REDCELL PRODUCTION
- 11. ERYTHROCYTE DIFFERENTIATION It isthe pathway through which an erythrocyte matures from a hemocytoblast into a full-blown erythrocyte. 01 Erythrocyte differentiation takes place in 8 stages. 02 The first seven all take place within the bone marrow. 03 After stage 7 the cell is then released into the bloodstream as a reticulocyte, where it then matures 1-2 days later into an erythrocyte: 04 Hemocytoblast, Proerythroblast, early & late erythroblast, Pronormoblast, normoblast, Reticulocyte 05
- 12. ERYTHROCYTE DIFFERENTIATION P.S. Hemocytoblastis a pluripotent hematopoietic stem cell
- 13. RED CELL PRODUCTION: ORIGIN Hemocytoblast: generalized stemcell, from which all blood cells form including both erythrocytes and leukocytes. (This is according to the monophyletic theory of blood cell formation) It resembles a lymphocyte and has a large nucleus; its cytoplasm contains granule
- 14. PATHOPHYSIOLOGY CONT. The primaryrole of red blood cells is the transport of respiratory gasses. In the lung, oxygen diffuses across the alveolar barrier from inspired air into blood, where the majority is bound by haemoglobin to form oxy-Hb, a process called oxygenation. Haemoglobin is contained in the red blood cells, which, being circulated by the cardiovascular system, deliver O2 to the periphery where it is released from its Hb-bond (deoxygenation) and diffuses into the cells. In anaemia, there is decreased Haemoglobin which decreases exercise performance despite a compensatory actions such as increase in cardiac output.
- 15.
- 16. CLINICAL FEATURES: NON-SPECIFIC Fatigue /malaise Dizziness / faintness Poor concentration Headache SOB Palpitations Angina
- 17. CLINICAL FEATURES:SPECIFIC Blood loss(PR, PV bleeding) Drugs (NSAIDS, chloramphenicol, phenytoin) Diet (vegans, alcoholics, elderly) Gastrectomy Pregnancy Chronic disease Ethnicity – Thalassaemia
- 18. SYMPTOMS OF ANAEMIA,CONTD
- 19. SYMPTOMS OF ANAEMIA,CONTD
- 20.
- 21. INVESTIGATIONS Rule out dilutionalanaemia (low Hb. due to increased effective circulating volume) FBC with differential (Hb, note WCC and platelets) Note mean corpuscular volume (MCV) and Red Cell Distribution Width (RDW) Reticulocyte count Blood film Rule out gastrointestinal disease in iron deficiency anaemia Additional laboratory investigations as indicated (Microcytic Anaemia, Normocytic Anaemia, Haemolytic Anaemia and Macrocytic Anaemia)
- 22. INVESTIGATIONS CONT. Reticulocyte studies(marrow activity) Reticulocyte count: N = 0.5 – 2 % of RBC’s RPI (Retic Production Index ) 1-2 = adequate BM response <1 = inadequate BM response >3 = haemolysis, haemorrhage Screen for (intravascular) haemolysis if suspected Raised LDH Decreased Haptoglobin Increased serum bilirubin (unconjugated) + urine urobilinogen
- 23. INVESTIGATIONS CONTD. Iron studies Folateand Vitamin B12 levels Bone Marrow For further Investigation of abnormal blood results. Can tell cellularity of marrow, type of erythropoiesis (micro/macrocytic), cellularity of cell lines, iron stores. Occult blood in stools GI Endoscopy Schilling test (macrocytic) Microcytic
- 24. MEAN CORPUSCULAR VOLUME (MCV) Theanaemia may be: Microcytic (MCV <80 fL): serum iron studies should be performed Normocytic (MCV 80-100 fL): the reticulocyte count should be examined to determine whether the anaemia is hypoproliferative (<2%) or hyperproliferative (>2%) Macrocytic (MCV >100 fL): the peripheral smear should be examined for megaloblasts and hypersegmented neutrophils. If these cells are present, the anaemia is megaloblastic. If they are absent, the anaemia is non- megaloblastic.
- 25.
- 26.
- 27. PERIPHERAL SMEAR Burr cells:irregularly shaped cells (uraemia) Anisocytosis: variation in cell size (megaloblastic anaemia, thalassaemia) Poikilocytes: variably shaped cells (Fe def anaemia) Rouleaux formation: red cells stack on each other (high ESR) Schistocytes: fragmented red cells (intravascular haemolysis) Spherocytes: spherical red cells (haemolysis, hereditary spherocytosis) Target cells: central staining, ring of pallor, outer rim of staining (liver dz. Sickle cell dz. Small amounts in Fe def.)
- 28. NORMAL A normal peripheralblood smear indicates the appropriate appearance of red blood cells, with a zone of central pallor occupying about 1/3 of the size of the RBC See also Neutrophil and few platelets
- 29. SEVERE IRON DEFICINECY Severe irondeficiency anaemia showing hypochromic pale haemoglobin-deficient microcytic small and misshapen red blood cells in human peripheral blood smear Variation in size (anisocytosis) and shape (poikilocytosis)
- 30. RETICULOCYTOSIS Reticulocytosis There is anincrease in reticulocytes, immature red blood cells. It is commonly seen in anaemia, particularly in haemolysis. They are seen on blood films when the bone marrow is highly active in an attempt to replace red blood cell loss (N = 0.5-2%)
- 31. SCHISTOCYTES The presence ofschistocytes (fragmented red blood cells) on the peripheral blood smear. It suggests red blood cell injury from damaged endothelium It is a characteristic feature of microangiopathic haemolytic anaemia.
- 32. SPHEROCYTOSIS Spherocytosis is anauto- haemolytic anaemia (a disease of the blood) characterized by the production of spherocytes (red blood cells (RBCs)) or erythrocytes that are sphere-shaped rather than bi-concave disk shaped. Usually hereditary or in autoimmune conditions
- 33. Harrison’s Principles ofInternal Medicine, 17th Edition CALCULATION OF RPI
- 34.
- 35.
- 36.
- 37. CLASSIFICATION: MORPHOLOGICAL 3 Major Types Microcytic hypochromic Macrocytic normochromic Normocytic normochromic
- 38.
- 39. CLASSIFICATION: MORPHOLOGICAL CONT. Normochromic, normocyticanaemia (normal MCHC, normal MCV). These include: anaemias of chronic disease haemolytic anaemias (those characterized by accelerated destruction of RBC's) anaemia of acute haemorrhage aplastic anaemias (those characterized by disappearance of RBC precursors from the marrow) (The mean corpuscular haemoglobin concentration (MCHC) is the average concentration of haemoglobin in the red blood cells. While Mean corpuscular volume (MCV) is the average volume of red cells.)
- 40. CLASSIFICATION: MORPHOLOGICAL CONT Hypochromic, microcyticanaemia (low MCHC, low MCV). These include: iron deficiency anaemia thalassemias Normochromic, macrocytic anaemia (normal MCHC, high MCV). These include: vitamin B12 deficiency folate deficiency
- 41.
- 42. MICROCYTIC HYPOCHROMIC MCV <80-100 MCHC<32-35 Causes: Fe-deficiency Anaemia of chronic disorders Thalassaemia Sideroblastic anaemia
- 43. IRON DEFICIENCY ANAEMIA Most commonform of anaemia Iron deficiency anaemia develops when body stores of iron drop too low to support normal red blood cell (RBC) production. Inadequate dietary iron, impaired iron absorption, bleeding, or loss of body iron in the urine may be the cause
- 44. AETIOLOGY Increased demand Increasedphysiological need for iron in the body e.g. pregnancy Increased losses haemorrhage obvious causes - menorrhagia in young women occult - peptic ulcer disease, GI cancer intravascular haemolysis paroxysmal nocturnal hemoglobinuria (PNH) cardiac valve RBC fragmentation
- 45. AETIOLOGY Decreased supply: dietarydeficiencies (rarely the only etiology) cow's milk (infant diet) "tea and toast" diet (elderly) absorption imbalances post-gastrectomy malabsorption (IBD of duodenum, celiac disease, atrophic gastritis)
- 47. CLINICAL FEATURES iron deficiencymay cause fatigue before clinical anaemia develops symptoms of anaemia: fatigue, weakness, irritability, exercise intolerance, syncope, dyspnoea, headache, palpitations, postural dizziness, tinnitus, feeling cold, confusion/loss of concentration
- 48. CLINICAL FEATURES brittle hair,nail changes [koilonychia (spoon-shaped)] dysphagia (e.g. oesophageal web, Plummer-Vinson ring) pallor - conjunctiva, palmar creases glossitis angular stomatitis (inflammation & fissuring at mouth corners) pica (appetite for non-food substances: ice, paint, dirt)
- 50. INVESTIGATIONS History Peripheral smear Poikilocytosis(variation in shape), anisocytosis (variation in size) and target cells Fe studies Fe: LOW Transferrin (iron transport protein): HIGH Transferrin saturation: LOW Ferritin (iron storage protein): LOW Often, the platelet count is elevated (>450,000/µL); this elevation normalizes after iron therapy
- 51. MANAGEMENT Find and treatthe cause Oral ferrous iron salts most economical and effective medication Ferrous sulfate most commonly used 200mg po TDS To promote absorption, patients should avoid tea and coffee and may take vitamin C (500 units) with the iron pill once daily Reserve parenteral iron for patients who are either unable to absorb oral iron or who have increasing anaemia despite adequate doses of oral iron
- 52.
- 53. ANAEMIA OF CHRONICDISEASE Causes include Chronic Infections: TB, IE, osteomyelitis Chronic inflammatory disease: RA, SLE Malignancy
- 54. MECHANISM Decreased release ofFe from BM stores to developing erythroblasts Inadequate EPO response to anaemia Decreased RBC survival - Inflammatory cytokine mediated
- 55. ANAEMIA OF CHRONICDISEASE Fe studies Serum Fe: LOW Ferritin: HIGH/N Transferrin: LOW/N Transferrin sat: LOW Management: Cause
- 56. MANAGEMENT OF ANAEMIAOF CHRONIC DISEASE IN PATIENTS WITH THE HUMAN IMMUNODEFICIENCY VIRUS Correct the underlying cause Treatment of nutritional deficiencies (iron, folic acid, vitamin B12) Treat opportunistic infections If drug-induced, discontinue & equally effective alternative Treatment with HAART improve anaemia in some patients with HIV Symptomatic treatment for HIV-related anaemia of chronic disease should be based on the patient's symptoms and cardiopulmonary status rather than on a specific haemoglobin concentration Blood transfusions and r-HuEPO (Recombinant Human Erythropoietin)
- 57.
- 58.
- 59. MACROCYTIC NORMOCYTIC ANAEMIAS CONT Megaloblastic– in BM, erythroblasts with delayed nuclear maturation that defective DNA synthesis. Megaloblastic anaemia results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the growth stage to the mitosis stage
- 60. MACROCYTIC NORMOCYTIC ANAEMIAS Non-megaloblastic macrocyticanaemias are disorders associated with increased red cell membrane surface area Such as pathologies of the liver and spleen which produce codocytes or "target cells" which have a central collection
- 61.
- 62. MEGALOBLASTIC: CAUSES Vitamin B12deficiency Malabsorption (need Intrinsic factor from stomach + intact terminal ileum for absorption) Pernicious anaemia Intestinal lesions (malignancy, TB, coeliac disease) 2. Poor dietary intake
- 63. MEGALOBLASTIC: CAUSES Folic aciddeficiency 1. Poor dietary intake 2. Increased demand Pregnancy Incr. cell turnover (haemolytic anaemia) 3. Malabsorption Resection of small bowel 4. Interference with utilization Drugs: Phenytoin, Methotrexate, Pyrimethamine, Trimethoprim
- 64. PERNICIOUS ANAEMIA Atrophy ofgastric mucosa – failure of IF production – vit B12 malabsorption Cause Autoimmune Parietal cell Ab in 90% Familial factor Schillings (absorption test)
- 65. MANAGEMENT Vitamin B12 deficiency Hydroxocobalamine imi Vit B12 IMI Vit B12 PO Folate deficiency Folic acid 5mg dly
- 66. NON-MEGALOBLASTIC Normoblastic BM: Causesof normoblastic BM with macrocytic anaemia Alcohol Liver disease Aplastic anaemia Reticulocytosis Marrow infiltration Myxoedema Myelodysplasia
- 67. NON-MEGALOBLASTIC Normocytic Normochromic Haematological disorders(aplastic anaemia, haemolytic anaemia) Chronic disease Endocrine disorders (hypothyroidism, hypoadrenalism) Acute blood loss Renal failure
- 68.
- 69. PANCYTOPENIA Definition: a decreasein all hematopoietic cell lines Anaemia, thrombocytopenia and leukopenia. Clinical Features • anaemia - fatigue • leukopenia - recurrent infections • thrombocytopenia - mucosal bleeding and ecchymoses
- 70. PANCYTOPENIA: CAUSES BM failure Ineffectivehaemopoesis (Megaloblastic anaemia) BM Suppression (Cytotoxic drugs) BM Infiltration (Malignancy) Myelofibrosis(myelodysplasias) Peripheral Consumption Stem Cell Defect (Aplastic anaemia) Hypersplenism
- 71. PANCYTOPENIA: INVESTIGATIONS FBC anddifferential, blood film investigate secondary causes: HIV test, serum B12, RBC folate, ANA often requires bone marrow biopsy to determine cause
- 72.
- 73.
- 74. APLASTIC ANAEMIA Syndrome ofbone marrow failure characterised by peripheral pancytopenia and marrow hypoplasia.
- 75. APLASTIC ANAEMIA Clinical features Anaemia Neutropenia Overtand/or recurrent infections Thrombocytopenia Haemorrhages, purpura Gingival bleeding, petechial rashes
- 76. CAUSES Acquired (more than80% of cases are acquired) Idiopathic factors Infectious causes: Hepatitis, Epstein-Barr virus (EBV), HIV, parvovirus, and mycobacteria Toxic exposure to radiation and chemicals, such as benzene Transfusional graft versus host disease (GVHD) Pregnancy Anorexia Severe nutritional deficiencies (B12, folate)
- 77. CAUSES CONT. Paroxysmal nocturnalhaemoglobinuria (PNH) Myelodysplastic syndrome (MDS Acute lymphoblastic leukaemia (ALL)(rarely) Drugs and elements (eg, chloramphenicol, phenylbutazone, gold) Hereditary Fanconi anaemia
- 78. INVESTIGATION & MANAGEMENT Investigations RPI:LOW BM: hypoplastic /aplastic with almost no haemopoietic precursors Management BM transplant Immunosuppressive therapy (if immune mediated cause)
- 79.
- 80.
- 81. INDICATIONS FOR REDCELL COMPONENTS: ANAEMIA Anaemia The aetiology of the anaemia should be investigated and, as far as possible, a definitive diagnosis should be made in every case. Medical management will be determined by the cause of the anaemia. Appropriate alternatives to blood transfusion must be considered. Consider transfusion in normovolaemic patients only if they are severely symptomatic e.g. shortness of breath at rest, angina, incipient cardiac failure. Patients with a Hb level below 8 g/dl should be considered for a transfusion. In chronic nutritional anaemias, a Hb of 6 g/dl is often well tolerated without associated medical complications and should respond well to treatment of the deficiency without transfusion being required.
- 82. INDICATIONS FOR REDCELL COMPONENTS Acute blood loss Acute blood loss of greater than 30% of blood volume (about 1 200-1 500 ml of blood in an adult) will often result in the need for a red cell transfusion. There must be no delay in ordering blood in situations where blood loss is acute and rapid or where there is a possibility of recurrence or continuation of bleeding. Limited volumes of crystalloid solutions should be used initially in volume resuscitation.
- 83. INDICATIONS FOR REDCELL COMPONENTS General surgery Consider transfusion if: • The pre-operative Hb level is less than 8 g/dl and the surgery is associated with major blood loss (>500 ml). • The intra- or post-operative Hb falls below 7 g/dl. A higher Hb level may be indicated in patients who are at risk for myocardial ischaemia or who are >60 years of age. Pre-operative anaemia must be investigated in every case, as medical management to raise the Hb level may be more appropriate than transfusion.
- 84. INDICATIONS FOR REDCELL COMPONENTS Anaemia in Acute Coronary Syndromes (ACS) In patients with ACS the guidelines cannot recommend for or against a liberal or restrictive RBC transfusion threshold. Transfusion to a Hb level between 8 and 10 g/dl should be considered acceptable, but the effect of each unit transfused must be evaluated for the risk of heart failure due to fluid overload. Obstetric haemorrhage During an obstetric haemorrhage, RBCs should be administered to maintain the patient free of signs and symptoms of inadequate tissue oxygen delivery. The Hb should be maintained between 6 and 10 g/dl during the resuscitation phase. Special attention must be given to maintaining adequate fibrinogen levels.
- 85. INDICATIONS FOR REDCELL COMPONENTS Cardiac surgery Pre-operative clinical variables have been identified that independently predict the likelihood of exposure to blood transfusion of patients undergoing cardiac surgery. These variables include: pre-operative Hb, weight, female gender, age, non-elective procedure, pre-operative creatinine levels, previous cardiac surgical procedure, and non- isolated procedure (e.g. coronary artery bypass graft (CABG) and valve repair). They constitute the clinical predictive index (TRUST). Making use of this scoring tool enables clinicians to stratify patients according to their likelihood of exposure to blood transfusion. It provides patients with important information about their transfusion-related needs, helps the medical team anticipate the patient’s transfusion needs, and guides the clinician in the ordering of additional tests.
- 86. PROCEDURE Collect blood forcrossmatch Identify that blood is correct for patient and that blood is ideally at room temp. Use a blood administration set Close observation for 1st 10 min for any reactions and thereafter continue close observation. Transfusion of a unit should occur within 6hours 1 U will increase Hb by 1,5-2g/dl
- 87. COMPLICATIONS: EARLY (<24HRS) Acutehaemolytic reaction (ABO, Rh incompatibility) Anaphylaxis Bacterial contamination Febrile reaction (from HLA Abs) Allergic reactions Fluid overload Transfusion related lung injury (ARDS due to anti-leukocyte Ab in donor plasma.)
- 88. COMPLICATIONS: DELAYED (>24HRS) Infections (hepB/C, HIV, bacteria) Fe overload Graft vs host disease Post transfusion purpura (decreased platelet count)
- 90.