Haematology + oncology
Haematology + oncology
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Guidance to Approaching Preparation from First Aid 2025:
Haematology should always be viewed in close relation to immunology
The different types of anaemia are high yield, as is being able to interpret blood smears
Knowing mechanisms and adverse effects of oncologic drugs is higher yield the details of clinical uses
Erythropoesis
The sites of erythropoiesis are different in the developing foetus.
Erythropoiesis in the:
yolk sac (3-8 weeks),
liver (6 weeks -> birth)
spleen (10 -> 28 weeks)
bone marrow (18 weeks -> adult)
Acronym: Young Liver Synthesises Blood
Haemoglobin
Embryonic globins are zeta and epsilon.
Foetal haemoglobin has two alpha, two gamma
Adult haemoglobin mostly has two alpha, two beta
HbA1 (α2β2)
HbA2 (α2δ2) is minor type of adult haemoglobin minor type of adult hemoglobin, typically 2-3% of the total Hb. Elevated HbA2 level often signals beta-thalassemia trait.
Haemoglobin is found in two states - a tense state and a relaxed state. The tense (T) state has a conformation that is not favourable for O2 binding. The relaxed (R) state is a conformation that is more favourable for O2 binding.
2,3-bisphosphoglycerate (2,3-BPG) is an allosteric effector that binds strongly to and stabilises the T-state of haemoglobin. This decreases haemoglobin's affinity for oxygen, facilitating oxygen release to tissues by shifting the oxygen dissociation curve to the right. Foetal haemoglobin binds less effectively to 2,3-BPG, allowing the capture of O2 from maternal haemoglobin.
Blood Grouping
AB is a universal recipient
O is a universal donor
Rh+ has the D antigen on the surface of red blood cells
A and B blood groups have only IgM antibodies; O blood group has both IgG and IgM
Rh- expresses anti-D of IgG subtype
Individuals naturally develop anti-ABO antibodies against the A and/or B antigens they lack, but they do not have pre-formed antibodies against the RhD antigen (the most significant Rh antigen) unless they have been previously exposed.
In haemolytic disease of the foetus and newborn, foetal red blood cells are destroyed due to blood group incompatibility, primarily involving Rh and ABO blood types. Minor blood group incompatibilities can also lead to disease.
Rh incompatibility usually affects subsequent pregnancies because maternal sensitisation occurs during the first pregnancy, leading to more severe complications such as in later pregnancies.
In the first pregnancy, mother is exposed to foetal blood (often during delivery) resulting in formation of maternal anti-D IgG
In subsequent pregnancies, anti-D IgG crosses the placenta and attacks foetal and newborn red blood cells, leading to haemolysis.
Severe complications can include intrauterine hydrops fetalis (excessive fluid build-up in foetus), jaundice shortly after birth, kernicterus (abnormally high bilirubin causing permanent brain damage)
Standard protocol is to administer anti-D IgG to an Rh- mother during their third trimester and within 72 hours of delivering an Rh+ baby.
Also appropriate in ectopic pregnancy, miscarriage, abdominal trauma, and antepartum hemorrhage to prevent maternal IgG production.
ABO incompatibility can impact the first pregnancy since maternal antibodies preexist. Usually less severe than Rh incompatibility.
A type O pregnant patient has a type A/B/AB foetus
Mother anti-A/anti-B IgG cross the placental and attack foetal/newborn red blood cells, leading to haemolysis.
There is mild jaundice in the neonate within 24 hours of birth
Treatment via phototherapy or exchange transfusion
KEL gene encodes a type II transmembrane glycoprotein -> highly polymorphic Kell blood group antigen.
Kell antigens are peptides found within the Kell protein, which is a transmembrane endopeptidase responsible for cleaving endothelin-3
The Kell antigens are K, k, Kpa, Kpb, Jsa and Jsb -> also targets for immune diseases which destroy red blood cells
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