Summary of Anaemias
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Clinical features
Blood loss: GI bleeding (peptic ulcer, diverticulitis), Menorrhagia, hookworm (developing countries)
Poor Diet
– Brittle hair + nails
– Atrophic glossitis
– Angular stomatitis
– Koilonychia
– (Rare: post- cricoid webs)
Hb ↓, ↓MCV
RBC microcytic, hypocgromic, anisocytosis, poikilocytosis.
-Serum ferritin ↓
-Serum Iron ↓
– TIBC ↑
Treat underlying cause.
– Oral iron – ferrous sulphate (SE = constipation)
Diseases: infection, colloagen vascular disease, rheumatoid arthritis, malignancy, renal failure, chronic inflammatory disease (crohns), TB, endocarditis.
↓ release of iron from bone marrow to developing erythroblasts, inadequate erythropoietin response to the anaemia, ↓RBC survival.
Normochromic, normocytic or microcytic anaemia
– ↓serum iron levels
– ↓ serum iron binding capacity
– ↑or normal serum ferritin.
– Treat underlying cause
– If due to renal failure then anaemia partly due to erythropoeitin deficiency – thus recombinant erythropoietin is useful.
 – Acquired
·         2* to myelodysplasia,
·         alcohol,
·         lead or isoniazid poisoning,  
·         idiopathic,
·         malignancy,
·         anti- TB drugs,
·          – malabsorption
There is iron available but the body is unable to synthesize it into the RBCs’
·         Dyserythropoiesis (defective developement of eyrocytes)
·         iron loading bone marrow
·          haemosiderosis (storage of iron compound – haemosiderin in various places e.g. endocrine, liver, cardiac damage)
Disorder of haem synthesis:
·         refractory anaemia
·         hypochromic cells in the peripheral blood
·         ring sideroblasts in bone marrow. (erythrocytes with granules of iron in their cytoplasm)
– Withdraw causative agents
– some response to pyridoxine (Vit B6)
– Maybe transfusion dependent and iron overload is a problem.
See haemolytic anaemias
Macrocytic  – Macrocytosis – presence of abnormally large red blood cells in the blood
Clinical Features
The presence in the bone marrow of developing RBCs with delayed nuclear maturation relative to that of the cytoplasm.
– defective DNA synthesis,
– ↓WC  (leukopenia)- may be hyper-segmented,
– ↓ platelets (thrombocytopenia)
– B12/ Folate deficiency
– Drugs (hydroxycarbamide/ hydroxyurea)
– Usually asymptomatic as the fall in the levels of Hb in response to the falling levels of B12/ folate occur over a long period of time therefore allowing the body to adjust.
Blood film: 
– hypersegmented polymorphs (B12 ↓), target cells (liver disease).
– Malignancy
– T4
– Serum B12 and serum folate/ red cell folate.
Bone marrow biopsy if above unsignificant:-
B12/folate deficiency, cytoxic drugs
Normoblastic marrow
– liver damage, myoxedema (coarsening of skin due to hypothyroidism)
Increased erythropoiesis
– e.g. haemolysis
Abnormal erythropoiesis
sideroblastic anaemia,
leukaemia, aplasia.
Vit B12 Deficiency
Diet: If no animal products are consumed (vegan)
Impared absorption:
Pernicious anaemia,
– Gastrectomy   (no IF from terminal ileum),
illeal disease/resection, coeliac disease.
Peripheral neuropathy – dorsal column degen.

(Rarely – dementia)

– Treat cause
– IM B12 injections

NB confirm whether B12 or folate deficient as folate will correct Hb in B12 deficiency but will not treat neuropathy

Pernicious anaemia
Autoimmune condition where there is atrophy of the gastric mucosa, with failure of Intrinsic Factor (and acid production)→ B12↓ absorption.
– usually older people,
–  ↑common in women, fair hair blue eyes.
– Associated with other autoimmune conditions:
 e.g. Thyroid,
– Glossitis
– Angular stomatitis
– Mild jaundice
– weakness + tiredness
– Dysponea
– Mild Splenomegaly
– Fever
Neurological – fits with very low levels of B12 and in
Polyneuropathy – weakness, ataxia, paraplegia
Optic atrophy – dementia, visual disturbances.
Macrocytic anaemia
– MCV > 110 with hypersegmented neutrophil nuclei
– in severe cases leucopoenia and thrombocytopenia.
– Hb ↓
– WCC + Platelets ↓
– Serum B12 ↓ < 50ng
– Red cell folate ↓
– Serum autoantibodies. Parietal cell antibodies 90% , IF antibodies 50%.
– Serum Bilirubin ↑                     (↑ breakdown of haemoglobin, due to ineffective erythropoiesis in the Bone marrow)
– Schilling test
(to differenciate PA from small bowel malabsorption)
– Bone marrow exam
-Hypercellular BM with megaloblastic changes.
IM Hydroxocobalamin
– x2 weekly for 3 weeks to replenish body stores, 3 monthly for life.
– watch for hypokalaemia when tx begins – oral K+ may be required
Folate Deficiency
Poor Intake
– old age
– poverty
– alcohol excess
Sources = green veg, beans, whole grains, some breakfast cereals
– coeliac disease
– tropical sprue
Excess utilization
pregnancy, lacatation, prematurity
– chronic haemolytic anaemia, malignant and inflammatory diseases,
Anaemia symptoms
– Red cell folate ↓
– Serum folate ↓
– jejunal biopsy to look for small bowel disease.
– Tx of underlying conditon.
– Oral folic acid 5mg daily for 4 months, higher doses if due to malabsorption.
– Prophylactic folic acid is given to pts with chronic haemolysis and pregnant women.
Clinical features
Aplastic anaemia
 – deficiency of all cell elements of the blood,
– hypocellularity of the bone marrow
Idiopathic acquired (50%)
  Chemicals e.g benzenes
   Drugs e.g. cytotoxics, chemotherapy,  chloramphenicol, gold, insecticides, ionising radiation
Infections e.g. viral hepatitis, HIV
Resulting from deficiency of RBCs, WBCs, Platelets.
– Anaemia
– ↑ likelyhood of infection
– Bleeding
– Bruising
– Bleeding gums
– Mouth infections are common
FBC pancytopenia with low/ abscent reticulocytes.
Bone marrow exam –hypocellular marrow with ↑fat spaces.
Tx Cause:
Supportive care
– Transfusions of RBC, platelets
Antibiotic tx.
Poor prognosis:
– peripheral blood neurtophil count < 0.5 x10⁹/L
– peripheral blood platelet count < 20×10⁹/L
– reticulocyte count of <40×10⁹/L
If no recovery:
– Bone marrow transplantation
Immunosuppressive tx with antilymphocyte gobulin and ciclosporin (where BMT is not possible due to ↑GVHD risk)
Haemolytic anaemias overview
There is increased destruction of red cells and a reduction of circulating lifespan to which the bone marrow is unable to compensate for the increased loss.
This may be:
extravascular (within reticuloendothelial system) they are removed from the circulation as they are defective
intravascular (within blood vessels)e.g. due to trauma, complement fixation or other extrinisic factors.  
RBC membrane defect:
– Hereditary spherocytosis
– Hereditary elliptocytosis
Haemoglobin abnormlaities:
– Thalassaemia
– Sickle cell disease
RBC metabolic defects:
– Glucose-6-phosphate dehydrogenase defieciency
-Pyruvate kinase defeicency
– Autoimmune haemolytic anaemia
– Haemolytic transfusion reactions
-Drug induced
– Paroxysmal noctural haemoglobinuria
– Microangiopathic haemolytic anaemia
– March haemoglobinuria
– Infections (e.g. malaria)
– Drugs/chemicals
– Hypersplenism
– Trauma
– family history
– race
-previous anaemia
Is there significant haemolysis:-
Is there increased cell breakdown:-
– bilirubin↑ (unconjugated),
– urinary urobilinogen ↑,
 – haptoglobin↓.
Is there increased red cell production:-
e.g. reticulocytosis,
-marrow hyperplasia.
Is the haemolysis mainly intra/extra vascular:-
E: → splenic hypertrophy
I: methaemalbuminaemia,
– free plasma haemoglobin,
– haemoglobinuria,
– ↓haptoglobin,
– haemosiderinuria.
-Urinary urobilinogen.
Blood films:polychromasia, macrocytosis, spherocytes, elliptocytes, fragmented cells or sickle cells.
Direct Coombs’ test: identifies RBCs coated with antibody/complement and a positive result ususally indicates an immune cause.
Chromium labelling: for RBC lifespan and the major site of breakdown
Multiple gene defects → ↓ rate of production of one or more globin chains.
The imbalance of globin chain production leads precipitation of globin chains within red cells or precursors. This → cell damage, death of RBC precursors in the bone marrow and haemolysis.
α thalassaemia: reduced α chain synthesis
β thalassaemia: reduced β chain synthesis
Symptoms may be mild–severe, depending on how many α/β chain genes have been deleted
– Film
– Iron
– HbA2
– HbF
– Hb
– Electrophoresis
Transfusion keep Hb >9g/dL
Iron chelators e.g. desferrioxamine. To protect against cardiac disease & DM.
↑ doses of ascorbic acid (vitamin C) also ↑iron output
– Splenectomy , if hypersplenism px.
– Folate supplements
Sickle cell anaemia
Inheritance of the β-globin gene.
May have:
sickle cell anaemia HbSS
sickle cell trait HbAS
HbSC – one S haemoglobin and one C haemoglobin group, (the C group causes the red blood cells to develop).
HbAS – there are usually no symptoms unless the patient is exposed to extreme hypoxia
HbAC – a milder course of HbSS but there is a ↑likelyhood of thromboses occuring.
HbSS – symptoms due to haemolysis and vaso-occlusion.  As the sickled cells are fragile and haemolyse and block small vessels.
…continued in large box below….
– ↓ Hb
– ↑ Reticulocyte count
– Bilirubin may be raised
– Blood film shows sickled erythrocytes
 Viz electrophoresis showing 80-90% HbSS and absent Hb A.
Folic acid in patients with severe haemolysis
pneumococal vaccine to infection risk, daily oral penecillin
Exchange transfusions to ↓ frequency of crises
Hydroxycarbamide (hydroxyurea) raises the conc of fetal Hb
– possible BMT
– mild anaemia (usually no symptoms due to hyperdynamic circulation and a lower O2 affinity of HbS than normal Hb).
– jaundice
– painful swelling of hands and feet
– recurrent sickle cell crises
– recurrent haemolysis → formation of pigment gallstones
A vascular necrosis of BM results in the bone marrow pain crisis, may be precipiated by hypoxia, dehydration or infection
– usually affects ribs, spine, pelvis in adults
– hands and feet (dactylitis) in children
– may require addmission to hospital for analgesia
Other complications:-
– Splenic atrophy
resulting in ↑infection risk with Pneumococcus, Salmonella species and Haemophilus
– Cerebral infection
causing fits and hamiplegia
– Retinal ischaemia,
may precipitate proliferative sickle retinopathy and visual loss.
renal papaillary necrosis
– leg ulcers
acute chest syndrome (commonest cause of death in adults with sickle cell )
   – fever
   – cough
   – dysponea
   – pulmonary infarcts on the CXR
Caused by infection, fat emboli from necrotic bone marrow or pulmonary infarction due to sequestration of sickle cells


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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