Microcytic anaemia

Cards (15)

  • The mnemonic for remembering the causes of microcytic anaemia is “TAILS”:
     
    T – Thalassaemia
    A – Anaemia of chronic disease
    I – Iron deficiency anaemia
    L – Lead poisoning
    S – Sideroblastic anaemia
  • Microcytic anaemia is defined as anaemia with an MCV of less than 80. As there is a lack of haemoglobin (Hb), an extra division of red blood cells (RBCs) occurs to maintain adequate Hb concentration. This results in smaller and paler (hypochromic) RBCs. The most common cause of microcytic anaemia is iron-deficiency anaemia.
  • Iron deficiency anaemia
    -          Lack of iron – vital component of haemoglobin – mild symptoms such as fatigue, palpitations, dizzy, postural hypotension, pallor, koilonychia – can lead to cravings such as ice, dirt, starch.
    -          Chronic blood loss
    -          Dietary deficiency
    -          Malabsorption – coeliac disease
    -          Increased requirements during childhood or pregnancy
    -          Menorrhagia
    -          Hookworm – GI blood loss
  • Lab findings in IDA:
    ·       Low MCV <80
    ·       Serum iron: low
    ·       Transferrin saturation: low
    ·       Ferritin: low
    Total iron-binding capacity: high (there is an inverse relationship between ferritin and TIBC)
  • Sideroblastic anaemia
    Defective protoporphyrin synthesis which can be due to congenital or acquired causes.
    -          Congenital – deficiency of aminolevulinic acid synthestase
    -          Acquired – alcoholism, lead poisoning, vitamin B6 deficiency
     
    The lack of protoporphyrin prevents the formation of haem. This results in iron building up in mitochondria creating pathognomonic ringed sideroblasts.
  • Thalassaemia
    Thalassaemias occur due to inherited mutations affecting the globin gene. They can be further classified into the specific gene that is affected (alpha or beta), as well as the severity of the condition (major, minor or trait). People with the thalassaemia trait may be asymptomatic or have very mild symptoms, while thalassaemia major can be severe enough to require regular transfusions. The most frequent occurrences of thalassaemias are in the Mediterranean, Africa, Western and Southeast Asia, as well as India and Burma.
  • Thalassaemia seems to be protective against Plasmodium falciparum​ malaria, which is why the population distribution is so similar for the two conditions. Thalassaemias result in classic clinical features such as chipmunk facies and a crew cut appearance on X-ray.
  • Lab findings in thalassaemia:
    ·       Low MCV <80 (usually lower relative to iron deficiency anaemia)
    ·       Ferritin: normal (unlike the low ferritin found in iron deficiency anaemia)
    ·       Haemoglobin electrophoresis: abnormal
    ·       Positive genetic testing for HBB, HBA1 or HBA2
  • Microcytic anaemia is a blood disorder in which the red blood cells are too small due to a lack of haemoglobin. Haemoglobin, an iron-rich protein, binds to oxygen, delivering it throughout the body. With microcytic anaemia, smaller red blood cells carry less oxygen, which leads to low energy and fatigue.
  • Microcytic – Iron deficiency anaemia
    A colonoscopy and oesophagogastroduodenoscopy (OGD) are indicated for unexplained iron deficiency anaemia to exclude gastrointestinal cancer as a source of bleeding.
     
    Referrals
    2ww cancer referral:
    ·       If over 60 with IDA
    ·       If under 50 with rectal bleeding
  • Treatment of IDA
    ·       Treat menorrhagia
    ·       Stop NSAIDs
    ·       Advise iron-rich foods (dark green vegetables, iron-fortified bread, meat, apricots, prunes, raisins)
    ·       One tablet once a day of oral ferrous sulfate (200mg), ferrous fumarate or ferrous gluconate – continue treatment for 3 months after IDA is corrected to allow stores to be replenished.
    ·       Consider IV iron if they have malabsorption issue such as coeliac disease.
  • Taking iron supplements may cause adverse effects but they should settle down with time:
    ·       Constipation.
    ·       Diarrhoea.
    ·       Epigastric pain.
    ·       Faecal impaction.
    ·       Gastrointestinal irritation.
    ·       Nausea.
    ·       Black stools
    If they do experience adverse effects, discomfort may be minimized by taking the supplement with or after food or reducing the dose to alternate days.
  • ·       Recheck haemoglobin levels (full blood count) within the first 4 weeks of iron supplement treatment. The haemoglobin concentration should rise by about 20 g/L.
    ·       If there is a response, check the full blood count at 2–4 months to ensure that the haemoglobin level has returned to normal.
    ·       Once haemoglobin concentration and red cell indices are normal:
    ·       Continue iron treatment for 3 months to aid replenishment of iron stores, and then stop.
    ·       Then monitor the person's full blood count periodically — for example, at 3, 6, 12, and 24 months.
  • Consider an ongoing prophylactic dose in people who are at particular risk of iron deficiency anaemia.
    200 mg ferrous sulfate daily may be beneficial in some people who have:
    ·       Recurring anaemia (such as in an elderly person) and further investigations are not indicated or appropriate.
    ·       A diet which is unlikely to meet daily iron intake recommendations
    ·       Malabsorption — for example, coeliac disease.
    ·       Menorrhagia
    ·       Had a gastrectomy.
    ·       Pregnant women.
    ·       People undergoing haemodialysis.
  • Refer people for specialist assessment if there is a lack of response (that is, an increase of less than 20 g/L in the haemoglobin level) after 2–4 weeks. If the person has already had normal upper and lower gastrointestinal investigations for iron deficiency anaemia and the anaemia persists or recurs, consider testing for Helicobacter pylori, and eradicate if present.