1 / 49

By Tiffany Shaw MBChB II 2002

Approach to Anaemia. By Tiffany Shaw MBChB II 2002. Anaemia – Definition. Reduced Hb concentration in blood Compared to normal range for the particular gender + age NOT reduced red cell count (unlike leucopenia or thrombocytopenia, which is defined by low counts). Symptoms:

oakes
Download Presentation

By Tiffany Shaw MBChB II 2002

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Approach to Anaemia By Tiffany Shaw MBChB II 2002

  2. Anaemia – Definition • Reduced Hb concentration in blood • Compared to normal range for the particular gender + age • NOT reduced red cell count (unlike leucopenia or thrombocytopenia, which is defined by low counts)

  3. Symptoms: SOB on exertion Tiredness Headache Angina Signs: Pallor Tachycardia +/- Jaundice +/- Koilonychia +/- Splenomegaly +/- Sore corners of mouth Symptoms + Signs Depends on cause of anaemia

  4. Symptom + Signs • Koilonychia = nail change, usually seen in Fe deficiency. Nails become brittle, spoon shaped, and ridged. • Sore mouth corners = angular cheilosis, seen in Fe, B12, or folate deficiency. • Jaundice = due to increased bilirubin production as a result of increased haemolysis (haemolytic anaemia)

  5. Investigation for Suspected Anaemia Full Blood Count • Hb concentration • Haematocrit • Red cell count • MCV (mean cell volume) • MCH (mean cell haemoglobin) • White cell count • Differential white cell count (neutrophils, lymphocytes, monocytes, eosinophils, basophils) • Platelet count

  6. Investigation for Suspected Anaemia • Hb concentration: confirms anaemia + assesses severity • MCV: is this microcytic, normocytic, or macrocytic? • MCH: is this normochromic or hypochromic? • Other cell counts: is this isolated anaemia or pan-cytopenia? Microcytic = MCV < normal (76) Normocytic = MCV normal (76 – 96) Macrocytic = MCV > normal (> 96)

  7. Classification Based on MCV • Microcytic ~ • Fe deficiency • Thalasaemia • Sideroblastic • Chronic disease • Normocytic ~ • Chronic disease • Haemolysis • Marrow disease • Macrocytic ~ • B12 deficiency • Folate deficiency • Liver disease • Marrow disease • Haemolysis (MCV pushed up by reticulocytosis)

  8. Investigating Microcytic Anaemia Clue One --- Iron Studies • Serun Iron (free Fe) • Ferritin (stored Fe) • Iron Binding Capacity IBC (transferrin) NB: Transferrin is the iron binding protein in blood and amount of transferrin reflects capacity to bind Fe.

  9. Investigating MicrocyticAnaemia Thalasaemia, Sideroblastic: • Fe Deficiency: • Low serum Fe • Low ferrtin • Increased IBC • NB: Increased IBC kind of reflects body’s attempt to grab more Fe. • Chronic Disease: • Low serum Fe • Normal ferritin • Reduced IBC • NB: Problem here is a block in the utilisation of Fe. • High serum Fe • High ferritin • Normal IBC • NB: There are defects in Hb production, therefore excessive Fe.

  10. Investigating MicrocyticAnaemia Clue Two --- Blood Film Exam • Fe deficiency  Microcytes, Target cells, Pencil cells • Chronic disease  Variable, depends on cause • Thalasaemia  Microcytes, Target cells • Sideroblastic  Dimorphic (both normal RBC and microcytic ones), Siderotic granules in RBC

  11. Investigating MicrocyticAnaemia Clue Three --- Special Tests • Hb electrophoresis: for thalasaemia • DNA analysis: for hereditary causes (e.g. thalasaemia) • Bone marrow: sideroblastic anaemia shows ringed sideroblasts in marrow

  12. Investigating Normocytic Anaemia Clue one --- Reticulocyte Count • Increased  Haemolysis • Normal or decreased  Chronic disease Marrow disease

  13. Investigating Normocytic Anaemia Clue Two --- Other Cell Counts • Normal  Chronic disease probably • Abnormal  Marrow disease likely

  14. Investigating Normocytic Anaemia Clue Three --- Special Tests • Bone marrow biopsy for ? marrow diseases • Other tests for ? chronic diseases • U + E • Creatinine • LFT • Thyroid function …etc.

  15. Investigating Macrocytic Anaemia Clue One --- Reticulocyte Count • Increased  Haemolysis • Normal or decreased  B12 deficiency Folate deficiency Liver disease Marrow disease

  16. Investigating MacrocyticAnaemia Clue Two --- B12 / Folate Level • Low  Deficiency • Normal  Liver disease Marrow disease NB: For B12, folate, and Fe deficiency, further investigations must be made to determine the cause of deficiency, so that appropriate therapy can be instituted.

  17. Investigating MacrocyticAnaemia Clue Three --- Other Cell Counts • Normal  liver disease probably (confirm with LFT, liver u/s…etc.) • Abnormal  probably marrow disease (confirm with marrow biopsy…etc.)

  18. Fe Deficiency Physiology: • Source of Fe = both in animal + vegetable products • Animal Fe more easily absorbed • Site of absorption = proximal jejunum • Vit C enhances absorption • Daily loss = urine, skin, faeces, hair, menstrual blood loss

  19. Fe Deficiency Findings associated with Fe deficiency: • Anaemia (microcytic) • Koilonychia • Angular cheilosis • Glossitis • Hair thinning • Abnormal Fe studies (see before)

  20. Fe Deficiency Causes: • Blood loss • Increased demand • Inadequate intake • Malabsorption • Menorrhagia • GI bleed • Haematuria …etc.. • Pregnancy • Growth • Gastrectomy • Coeliac disease

  21. Fe Deficiency Mx: • Treat underlying cause if possible (e.g. bleed) • Oral Fe replacement – Ferrous sulphate best, gluconate second • Taken before meals TDS • Continue for 4-6/12 • Reticulocytosis typically begins 7 days after Rx • Fe replacement IV or IM if oral not possible

  22. Thalasaemia • Hereditary anaemia • Impaired production of components of the globin • Classified into a and b depending on which chain is deficient • Lack of a chain = a thalasaemia • Lack of b chain = b thalasaema

  23. a Impaired production of a chain in the globin. Severity depends on number of genes deleted 4/4 = hydrops fetalis (intrauterine death) 3/4 = haemoglobin H disease (severe anaemia) 1- 2/4 = a trait (mild anaemia) b Impaired production of b chain in the globin Major = complete failure of production (severe anaemia) Intermedia = partial failure (moderate anaemia) Minor = asymptomatic or mild anaemia Thalasaemia

  24. Diagnosis: Microcytic anaemia Blood film examination Hb electrophoresis DNA analysis Associated findings: Usual signs of anaemia Failure to thrive Hepatosplenomegaly Expansion of the skull High serum + storage Fe Thalasaemia

  25. Thalasaemia Mx: • Transfusion (packed red cells) prn • Iron chelation therapy with DFX • Splenectomy prn • Bone marrow transplantation (definitive Rx) • Genetic counseling

  26. Sideroblastic Anaemia • Defect of haem synthesis • Increased Fe present as granules arranged in a ring around nucleus of developing RBC in marrow (ringed sideroblasts) • Peripheral blood shows microcytic hypochromic RBC • May be hereditary or acquired

  27. Sideroblastic Anaemia Causes: • Hereditary type (X-linked) • Alcohol • Radiation therapy • Lead poisoning

  28. Sideroblastic Anaemia Mx: • Transfusion prn • Iron chelation therapy • Some benefit from Vit B6 (esp the hereditary type)

  29. Haemolytic Anaemia Common types: • Autoimmune • Alloimmune • G-6PD deficiency • Pyruvate kinase deficiency • Hereditary spherocytosis • Thalasaemia (discussed before) • Sickle cell anaemia Normocytic Microcytic

  30. Autoimmune • Autoantibodies against self RBC • Divided into warm + cold types, depending on which temperatures antibodies work best under • May be idiopathic or secondary to other conditions • +ve for direct Coomb’s test

  31. Warm Type Max at 37 degrees Ig G Get microcytosis + spherocytosis Splenomegaly common Cold Type Max at 4 degrees Ig M Autoimmune

  32. Warm Type Causes: Idiopathic c.t. disorder (SLE) CLL Drug induced (methyl dopa) Cold Type Causes: Idiopathic Infection (e.g. glandular fever, Mycoplasma infection) Lymphoma Autoimmune

  33. Warm type Mx: Steroids Transfusion prn Splenectomy if steroids fail Other immunosuppressives Cold type Mx: Avoid cold environment Immunosuppressives (chlorambucil, cyclophosphamide) Transfusion prn Autoimmune

  34. Alloimmune • Mismatched blood transfusion • Haemolytic disease of the newborn • Post bone marrow transplantation • Post organ transplantation

  35. Hereditary Spherocytosis • Hereditary anaemia • Most common one in Caucasian • Autosomal dominant • Defect in RBC membrane • RBC becomes spherical • Therefore destroyed prematurely in spleen • Splenomegaly common

  36. Hereditary Spherocytosis Special test --- Osmotic Fragility Test • Spherical RBC  increased volume : surface area ratio • More prone to lysis by osmosis • Measure degree of lysis of RBC in different concentrations of saline  spherical ones lyse more • Therefore confirm spherocytosis

  37. Hereditary Spherocytosis Mx: • Splenectomy to stop destroying RBC prematurely

  38. G-6PD Deficiency • G-6PD = enzyme required to generate ATP to maintain shape of RBC • Deficiency  RBC more susceptible to oxidation stress, e.g. ingestion of certain drugs / fava beans • Haemolysis occurs with such ingestion • Normal at other times

  39. 6-GPD Deficiency Mx: • Stop offending drugs / fava beans • Transfusion prn during attacks

  40. Physiology: Source of B12 = food of animal origin Storage = in liver, enough for 2 – 4 years Absorption = in terminal ileum Vit B12 ingested Binds to “R protein” in saliva, gastric juice IF secreted by parietal cells releases Vit B from R protein Form IF-Vit B12 complex Complex absorbed in terminal ileum Transcobolamin in plasma strips off Vit B12 and transport to tissues Vit B12 Deficiency

  41. Diagnosis: Macrocytic anaemia Low B12 level Associated findings: Features of anaemia Mild jaundice Glossitis Angular cheilosis Neuropathy (often tingling in feet +/- visual or psych disturbance) Vit B12 Deficiency

  42. Vit B12 Deficiency Causes: • Inadequate intake (e.g. vegan) • No IF (gastrectomy, pernicious anaemia) • Malabsorption (ileal resection, Crohn’s disease)

  43. Vit B12 Deficiency Pernicious Anaemia: • Autoandibodies develop against parietal cells or intrinsic factors • Therefore no IF • Can’t absorb Vit B12 • Peak incidence at 60 years old

  44. Vit B12 Deficiency Distinguish between no IF & ileal problems: • Hx (e.g. gastrectomy) • Test for autoantibodies against parietal cells or IF • Radioactive Vit B12 study Give radio-labelled Vit B12 +/- IF. IF corrects gastric problems, but not ileal problems.

  45. Vit B12 Deficiency Mx: • Correct underlying cause if possible (e.g. adequate intake) • IM Vit B12 injection • 6 injections to replace deficit (1 every 2 –3 days) • Maintenance (1 injection 3/12)

  46. Folate Deficiency Physiology: • Source = green vegetables + animal liver • Body store = 4/12 supply • Absorption = through proximal jejunum

  47. Diagnosis: Macrocytic anaemia Low folate level Associated findings: Features of anaemia Mild jaundice Glossitis Angular cheilosis No neuropathy!! Folate Deficiency

  48. Folate Deficiency Cause: • Inadequate intake • Malabsorption (coeliac disease, bowel resection) • Drug induced (anti-convulsant)

  49. Folate Deficiency Mx: • Treat underlying cause if possible (e.g. coeliac disease) • Folate replacement • Oral folate 5 mg OD for 4-6/12

More Related