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Haematology - PowerPoint Presentation

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  • Iron deficiency is the commonest cause of anaemia. Blood loss
  • Iron is best absorbed from the upper small bowel as ferrous state (Fe2+). It is transported across the intestinal cell and into the plasma. It Is carried to red cell in bone marrow by transferrin. Red cells have sTfR which can be measured in plasma
    Clinical feature – atropihic tongue vs beefy tongue in B12 deficiency
  • Ferritin is an acute phase reactant – its level increases with active inflammation, in the same way as ESR, CRP. sTfR reflects the true state of iron stores
    Iron overload – haemochromatosis and in conditions requiring frequent transfusions – serum iron and ferritin raised. TIBC is usually low.
    Iron deficiency: Brittle nails
    Koilonychia (spoon-shaped nails)
    Smooth tongue
    Angular stomatitis
    Glossitis
  • How absorbed
  • B12 def causes: most common – malabsorption. Small bowel disease: Crohn’s, coeliac disease
    Reduction in IF – post gastrectomy OR pernicious anaemia
    Pernicious anaemia – autoantibodies against gastric parietal cells and IF. Is an association with other autoimmune diseases (especially thyroid and Addison’s); Increased risk of gastric carcinoma
    Schilling test – if test is still abnormal after giving IF? Problem likely to be in ileum. Cause? Could be bacterial overgrowth. Therefore give antibiotics
  • Absorption more rare cause unless wide spread disease as folate is absorbed in duo and jej
    NEUROPATHY DOES NOT OCCUR
  • Intravascular haemolysis: low haptoglobins, haemosiderniuria
    Red cells are destroyed in blood vessels and Hb released. Haptoglobins bind to free haemoglobin and escort to liver.
    Haptoglobins become saturated and may be passed in urine or converted to haemosiderin. Alterantively, further reactions  methaemalbumin in circulation
    Polychromasia: “many colours” - blue tinge, caused by rRNA in young RBC and pink colour of Hb
    Reticulocytosis
  • G6PD deficiency affects all cells, but most severe in erythrocytes when pentose phosphate pathway provides only means of generating NADPH. Precipitating factors can cause symptoms with underlying G6PD deficiency e.g. Antibiotics, Antimalarials, Antipyretics
  • true (primary: PRV vs secondary: hypoxia: chronic smoking, altitude, lung disease; excess erythropoietin: renal cell ca, hepatocellular ca, polycystic kidneys) vs apparent (reduced blood volume)
    Excess erythropoietin: renal cell ca, polycystic kidneys, adrenal ca, hepatocellular ca
  • Pancytopenia: sepsis, SLE, aplastic anaemia
  • AML: Inc blast cells dec mature cells
    CML: Inc impaired mature
    ALL: Inc lymphoblasts NO maturation
    CLL: Inc mature abnormal, B- and T- cells
  • Pre-op assessment of bleeding
  • Lymphocytosis: primary (malignant clonal proliferation) vs secondary (infections: EBV, rubella, varicella zoster, TB; autoimmune)
  • 1. B. Lymphocytosis. Many viral infections, including infectious
    mononucleosis, cause a lymphocytosis.
    2. H. Reticulocytosis. The administration of haematinics results in
    a brisk increase in erythropoiesis with a transient rise in the
    peripheral blood reticulocyte count.
    3. A. Anaemia. There are several mechanisms that may result in
    anaemia in patients with chronic renal failure, the most
    important being a reduced production of erythropoietin. Other
    mechanisms include iron deficiency due to blood loss from the
    gastrointestinal or genitourinary tracts, folate loss into the
    dialysate and shortened red cell survival.
    4. G. Polycythaemia. Chronic hypoxia stimulates the production
    of erythropoietin causing an increase in the red cell mass.
    5. I. Thrombocytopenia. The intravascular coagulation depletes
    peripheral blood of platelets.
  • · Most likely diagnosis: Pernicious anemia.A. The two most common causes of megaloblastic anemia are deficiencies of vitamin B12 or folate. These deficiencies decrease the synthesis of DNA, which results in nuclear-cytoplasmic assynchrony in maturation, which is the hallmark of megaloblastic anemias. This abnormal maturation will produce characteristic histologic changes in the cells in the peripheral blood, including oval macrocytes and hypersegmented PMNs, which are neutrophils with more than five lobes to their nuclei.
  • Most likely diagnosis: Infectious mononucleosis.
    · Confirmatory laboratory tests:(1) Specific antibodies for Epstein-Barr virus (EBV) antigens (viral capsid antigens, early antigens, or Epstein-Barr nuclear antigen), (2) a positive heterophil reaction (monospot test), and (3) lymphocytosis with the characteristic atypical lymphocytes in the peripheral blood.
  • failure to thrive: poor weight gain and physical growth failure over an extended period of time
  • TIA: most common cause is an embolus that occludes an artery in the brain
    Polycythaemia rubra vera presented with TIA as blood viscosity increased by increased red cells and platelets become adhesive
  • B12 deficiency. Peripheral neuropathy. Big and beefy tongue
  • Transcript

    • 1. Haematology
    • 2. FBC • Red Cells: Hb, MCV • WBC: cell type and presence of abnormal or immature forms • Platelets
    • 3. Anaemia • Hb • MCV Microcytic Normocytic Macrocytic Iron def Thalessaemia ACD Acute blood loss Haemolytic Marrow infiltration ACD B12 Folate Alcohol Reticulocytosis Hypothyroid
    • 4. Haematinics • Deficiencies can cause anaemia: Iron B12 Folate Duodenum Terminal ileum Duo and jej
    • 5. Iron absorption
    • 6. Iron deficiency Intake vs Utilisation PubertyDiet Malabsorption not common • Blood loss • Atrophic tongue!
    • 7. IDA vs ACD Iron parameter IDA ACD Serum iron TIBC Serum ferritin Serum sTfR N
    • 8. B12 absorption
    • 9. B12 deficiency • Pernicious anaemia – autoantibodies • Neurological problems • Beefy tongue! • Schilling test – radioactive; im. With IF Not common Diet RARE Small bowel disease Reduction in IF Intake vs Utilisation
    • 10. Folate defiency Intake vs Utilisation • Neural tube defects • NO neuropathy Pregnancy Lactation Adolescence Excess turnover of cells: Haemolysis, malignancy Diet COMMON Coeliac disease Antifolate drugs
    • 11. Haemolytic anaemia • Intravascular vs Extravascular : bilirubin, LDH • Polychromasia, reticulocytosis Hereditory spherocytosis Thalassaemia Sickle cell anaemia G6PD deficiency Pyruvate kinase deficiency Damage to red cell membrane Malaria Oxidant damage Aquired vs Inherited
    • 12. G6PD deficiency • X-linked • Inability to detoxify oxidising agents • Heinz bodies, spherocytosis
    • 13. Polycythaemia True Apparent Primary: PRV Secondary Hypoxia: chronic smoking high altitude lung disease Excess erythropoietin Dehydration
    • 14. Production by Bone marrow Cell loss/ destruction Polycythemia 1. Haematinic deficiency 2. BM infiltration/failure • Haemopoietic cancer • Metastatic cancer • Aplasia Shortened survival bleeding haemolysis •Acquired (environment) •Immune •Microangiopathic •Malaria •**PNH • Inherited •Haemoglobin •Enzyme •Membrane RBC
    • 15. Reduced cell counts Three cell lines reduced/involved • Think bone marrow failure/infiltration (but don’t forget Vit B12/folate deficiency) One cell line reduced • Think increased destruction/loss (but don’t forget iron deficiency in low RBC/Hb)
    • 16. PlateletsProduction by Bone marrow Cell loss/ destruction Primary: CML Secondary: infection, inflammation, pregnancy, post-splenectomy 1. Drug induced 2. BM infiltration/failure • Haemopoietic cancer • Metastatic cancer • Aplasia Immune mediated Hypersplenism Disseminated intravascular coagulation
    • 17. • AML vs CML • ALL vs CLL
    • 18. ALL • Clinical features: - bone pain - hepatomegaly - splenomegaly - lymphadenopathy - thymic enlargement - testicular enlargemenrs - fatigue, lethargy, pallor, breathlessness (anaemia – normocytic, normochromic) - fever and infection features (neutropenia) - bruising, petechia, bleeding (thrombocytopenia) • Replacement of normal bone marrow by lymphoblasts
    • 19. Bleeding disorders
    • 20. Coagulation screen What do you get? Prothrombin time (± INR) Activated partial thromboplastin time (APTT) Thrombin time (TT)
    • 21. Haemostasis screening INR (Prothrombin Time) Measures extrinsic & common pathway Common abnormality warfarin liver disease DIC APTT Measures intrinsic and common pathway Common abnormality heparin liver disease DIC haemophiliaTT (thrombin time) Measures fibrinogen&thrombin inhibition Common abnormality DIC heparin
    • 22. What you need to know • normal ranges for WBC, Hb, MCV, platelet count in adults • If the WBC is abnormally high or abnormally low we expect you to be able to work out whether it is the count of neutrophils, lymphocytes or eosinophils that is causing the abnormality in the total WBC • We expect you know that there are variations in haematological normal ranges related to gender, age and ethnic origin
    • 23. Questions
    • 24. SBA • What event is this? • When is it? • When are you getting tickets?
    • 25. White cells • Neutrophilia: bacterial infections, inflammation, malignancy, necrosis, treatment with corticosteroids? • Neutropenia: post-chemo, viral, adverse drug reactions eg. carbimazole • Lymphocytosis: viral, lymphomas, chronic infections eg TB, chronic lymphocytic leukaemia • Eosinophilia: parasite infection, atopic allergic, Hodgkin
    • 26. EMQ • A Anaemia • B Lymphocytosis • C Lymphopenia • D Neutropenia • E Neutrophilia • F Pancytopenia • G Polycythaemia • H Reticulocytosis • I Thrombocytopenia • J Thrombocytosis 1. A patient with infectious mononucleosis. 2. A patient who has just started treatment with B12 and folate for megaloblastic anaemia. 3. A patient with chronic renal failure. 4. A patient with chronic obstructive pulmonary disease. 5. A patient with disseminated intravascular coagulation.
    • 27. SBA • A 61-year-old woman with pancytopenia, mild jaundice, and peripheral neuropathy is found to have decreased serum levels of vitamin B12. Which of the abnormal cell morphologies listed below is most likely to be present in a smear made from her peripheral blood? • A. Hypersegmented PMNs • B. Large granular lymphocytes • C. Oval microcytes • D. Pelger-Huet neutrophils • E. Plasmacytoid lymphocytes
    • 28. SQA • A 16-year-old girl has a sore throat, enlarged tender cervical lymph nodes, and low-grade fever for 3 days. In addition to erythematous pharyngeal mucosa and cervical lymphadenopathy, physical examination reveals mild splenomegaly. A complete blood count (CBC) shows an increased number of white blood cells with a lymphocytosis and many reactive lymphocytes. • What is the most likely diagnosis? • What laboratory tests would be helpful in confirming the diagnosis?
    • 29. SQA • 3 year old girl referred with failure to thrive. • Hepatosplenomegaly. • Hb 5.1 (13.0-16.5) • MCV 58 (80-100) • WCC 9.1 x 109 (4-11 x 109 ) • Platelets 317 x 109 (150-400 x 109 ) • Bilirubin 38 (1-22) • AST (19-48)
    • 30. SQA • 63 year old man presents with a left-sided TIA • Similar episode 1 week earlier. Results of FBC: • Hb 21.2 (13.0-16.5) • Haematocrit 0.61 • WCC 15.3 x 109 (4-11 x 109 ) • Increased neutrophils and eosinophils • Platelets 897 x 109 (150-400 x 109 ) • Bilirubin 8 (1-22) • AST 30 (19-48) • Cholesterol 3.6 (0.1-1.6)
    • 31. SQA • 78 year old man • Hepatolsplenomegaly • Hb 10.1 (13.0-16.5) • WCC 227 x 109 (4-11 x 109 ) • Platelets 741 x 109 (150-400 x 109 ) • Uric acid 490 (110-420)
    • 32. SQA • 58 year old woman with pallor, decreased sensation in both legs below the knee, absent ankle jerk • Hb 8.2 (13.0-16.5) • MCV 124 (80-100) • WCC 2.4 x 109 (4-11 x 109 ) • Platelets 102 x 109 (150-400 x 109 )