PY2.1-13 | Haematology — Summary & Reflection

REFLECT

Imagine you're a first-year resident in a busy Indian district hospital. A 22-year-old woman (gravida 2) is brought in after a postpartum haemorrhage. Her Hb is 5 g/dL, she is pale, tachycardic, and hypotensive.

Think through the physiology you've just learned:

1. Why is her heart beating fast? (Hint: reduced O₂ delivery → compensatory mechanisms)
2. Her blood group is O-positive. What blood can she safely receive? Why must you cross-match even if the ABO group matches?
3. After transfusion, her body will need to regenerate RBCs. What will trigger increased erythropoiesis? (Think: EPO, hypoxia sensing in the kidney)
4. She is also iron-deficient (ferritin 3 ng/mL). Why will oral iron alone be insufficient in the acute setting? What route would you use?
5. Two weeks later, her reticulocyte count is 5% (elevated). What does this tell you about her bone marrow response?

Now connect to your parallel subjects: In Anatomy, which bones contain the red marrow that will produce her new RBCs? In Biochemistry, which pathway provides the succinyl CoA needed for haem synthesis?

KEY TAKEAWAYS

Key takeaways — your study checklist:

1. Blood composition — plasma (55%, contains albumin, globulins, fibrinogen) + formed elements (45%, mainly RBCs). Haematocrit = PCV. Serum = plasma minus fibrinogen.
2. Haematopoiesis — HSC in bone marrow → myeloid (RBCs, WBCs, platelets) and lymphoid (lymphocytes). Sites: yolk sac → fetal liver/spleen → bone marrow (adults: flat bones).
3. Erythropoiesis — regulated by EPO from kidney in response to hypoxia. Requires iron, B₁₂, folate. Proerythroblast → reticulocyte → mature RBC.
4. RBC — biconcave disc, no nucleus, 120-day lifespan, spectrin-actin skeleton. Functions: O₂ transport (Hb), CO₂ transport, buffering.
5. Haemoglobin — quaternary protein (4 subunits × haem + globin). Types: HbA (α₂β₂, 97%), HbF (α₂γ₂, higher O₂ affinity). O₂-Hb dissociation curve: sigmoid, right shift (↑temp, ↑CO₂, ↑H⁺, ↑2,3-DPG) = Bohr effect.
6. Hb breakdown → biliverdin → unconjugated bilirubin → liver conjugation → bile → stercobilin (faeces) + urobilin (urine). Three types of jaundice.
7. Iron metabolism — absorption in duodenum (DMT1 for non-haem, haem carrier for haem), transport by transferrin, storage as ferritin. Hepcidin = master regulator (↑ hepcidin = ↓ iron absorption).
8. Anaemia classification by MCV — microcytic (iron deficiency, thalassaemia), normocytic (acute blood loss, CKD, haemolytic), macrocytic (B₁₂, folate deficiency).
9. WBCs — neutrophils (bacteria, 60-70%), eosinophils (parasites/allergy), basophils (histamine), lymphocytes (T, B, NK — immunity), monocytes (phagocytosis, APC).
10. Platelets — fragments from megakaryocytes, 8–12 day lifespan. Adhesion (vWF-GPIb) → activation → aggregation (GPIIb/IIIa-fibrinogen). Aspirin blocks COX-1.
11. Coagulation cascade — intrinsic (aPTT), extrinsic (PT/INR), common pathway. Thrombin = central enzyme. Vitamin K needed for factors II, VII, IX, X ('1972').
12. Natural anticoagulants — AT-III (enhanced by heparin), protein C/S (inactivate Va, VIIIa), TFPI. Fibrinolysis: tPA → plasmin → FDPs + D-dimers.
13. Blood groups — ABO (naturally occurring IgM antibodies), Rh (D antigen, antibodies only after exposure). HDN: Rh-negative mother + Rh-positive fetus → anti-D IgG → give RhoGAM. Acute haemolytic transfusion reaction = ABO mismatch = complement-mediated intravascular haemolysis.