Summary
Summary Haematology - Anaemias notes
- Module
- Haematology
- Institution
- University Of Westminster (UOW)
Iron Deficiency Anaemia, Megaloblastic Anaemias, Sickle Cell Trait and Anaemia, Thalassaemias, Haemolytic Anaemias,
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AnaemiasIron Deficiency Anaemia
● Hypochromic microcytic. MCV and MCH ↓
● Caused by defect in Hb synthesis
● Reasons for iron deficiency: limited ability for iron absorption, menses, poverty diet
● Diet iron exists in the ferrous state (Fe2+), haem, and the ferric state (Fe3+). The latter of which
is absorbed the least rapidly.
● Dietary iron absorption occurs through intestinal epithelial cells. Iron present in haem is
released by the intracellular enzyme haemoxygenase-1. Ferric iron is converted to ferrous
state through the divalent metal transporter-1. Intracellular iron is then transported to the
circulation by ferroportin.
● Transferrin + transferrin receptor (TfR) + ferritin mediate transport and storage of iron to the
erythroblast during haemopoiesis
● Hepcidin inhibits transferrin receptor and regulates the activity of ferroportin. Important
regulator of iron absorption pathway.
● Symptoms: painful glossitis, angular stomatitis, brittle spoon nails
● Cause in developing countries is a life-long poor diet. Diet deficient in iron rarely causes
anaemia in developed world
● Diagnostic tests: blood film, measure serum ferritin levels, tests should also find reason for
iron deficiency (diet, aspirin, blood loss ie menorrhagia, bowel dysfunction causing
haemorrhage
● Lab findings: RBC indices fall before anaemia occurs. Blood film can show
anisochromasia, target cells (uncommon; more common in thalassaemia),
poikilocytes, reticulocytes (uncommon; only if severe). Platelet count ↑ to
prevent blood loss. Hb and serum iron ↓ and total iron binding capacity ↑.
Contrasting results compared to other hypochromic anaemias.
● Diagnostic clinical features exclude physical appearance
● Treatment should treat the underlying cause. Usually orally administered in the form of
ferrous sulphate. Course of at least 6 months. Parenteral iron can be injected but is only for
severe iron deficiency
Megaloblastic Anaemias
● Vitamin B12 deficiency is usually caused by pernicious anaemia. Less commonly caused by
veganism.
● Occurs from severe malabsorption of B12 from diet. Takes 2 years to deplete stores and
develop.
● Vitamin B12 has a central cobalt atom. Humans cannot synthesise, need to ingest from
animal food
, ● Absorption of vitamin: B12: Protein-B12 → B12 → B12-IF → B12-IF-cubilin →
B12-IF-cubilin-amnionless → *endocytosis* → B12. (IF=intrinsic factor)
● Transport of vitamin B12: B12 in blood + TC plasma protein → B12-TC → bone
marrow. (TC=transcobalamin). Haptocorrin plasma protein binds to B12 but
does not transport to bone marrow.
● TC mutation causes megaloblastic anaemia but serum B12 appears normal as it is bound to
haptocorrin
● Pernicious anaemia is an autoimmune attack of mucosa, so intrinsic factor
secretion is lacking and haptocorrin levels rise. Antibody serum level against
IF ↑.
● B12 in form of methyl tetrahydrofolate (THF) is a coenzyme for homocysteine
→ methionine, important for DNA synthesis. DNA synthesis rate reduction,
decreases rate of maturation of RBC
● Deoxyadenosyl B12 assists in conversion of methylmalonyl CoA to succinyl CoA.
● Lab assays test for homocysteine and methylmalonic acid
● Folate deficiency is caused by inability to absorb folate.
● Cannot be synthesised. Needs to be ingested. As above ↑.
● During absorption, converted to methyl tetrahydrofolate (THF), coenzyme for methionine
synthesis
● B12 necessary to convert methyl THF → THF. THF is a substrate for folate
polyglutamate synthesis
● Cells convert folate to folate polyglutamates, used in amino acid interconversions and most
importantly coenzymes for dTMP and dTTP synthesis
● Folate deficiency inhibits thymidine monophosphate synthesis, a rate-limiting step in DNA
synthesis
● Clinical features: painful glossitis, angular stomatitis, weight loss. Long term: neuropathy,
spina bifida in newborns if mother is deficient
● Diagnostic tests: blood film, haematinic assays for B12 and red cell folate,
liver and thyroid function tests, antibody test for parietal cells if B12 ↓, bone
marrow aspirate if diagnosis cannot be confirmed
● Lab findings: MCV and MCH ↑, PCV ↓, FBC ↓, macrocytic, anisocytosis,
poikilocytosis, white cell and platelet count ↑, hypersegmented neutrophils,
hypercellular bone marrow with retarded nuclear maturation.
Sickle Cell Trait and Anaemia
● Caused by one point mutation on β-globin gene, glutamine → valine ie. HbA →
HbS (α2β2S)
○ No other mutations can cause what is referred to as SCD
● If both alleles are mutated, trait → anaemia (SCA)
● Mutated HbS is insoluble, forms crystals when exposed to low O2 tension and deoxygenated
HbS polymerises into long fibres (block blood vessels)
● HbS gives up oxygen to tissues more easily than HbA
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