Q3 LONG ANSWER 10M ★ High-yield

Classify blood groups. Describe the ABO and Rh systems and discuss mismatched transfusion reaction. Add a note on erythroblastosis fetalis.

Physiology · 1st Professional — Pre-Clinical

Introduction

Blood group = classification of blood based on the presence or absence of inherited antigens (agglutinogens) on the RBC membrane, with corresponding antibodies (agglutinins) in plasma.

Over 30 systems known; ABO and Rh are clinically the most important
ABO discovered by Karl Landsteiner (1901)

Abo System

Group	Antigen on RBC	Antibody in plasma	Frequency (India)
A	A	Anti-B	~22%
B	B	Anti-A	~33%
AB	A and B	None	~7%
O	None	Anti-A and anti-B	~37%

Antibodies are naturally occurring IgM — do not cross the placenta
Appear by 2–8 months of age; peak at 8–10 years
Antigens are glycoproteins; the precursor is the H antigen
Bombay phenotype (Oh) — no H antigen → tests as O but cannot receive O blood

Inheritance

Three alleles — IA, IB, i
IA and IB are co-dominant; i is recessive
Group A = IAIA or IAi; Group O = ii only

RH System

Discovered in the Rhesus monkey by Landsteiner and Wiener
Antigens — C, D, E, c, e; D is the most antigenic
Rh positive = D antigen present; 85% of Indians are Rh positive
Anti-D is not naturally occurring — forms only after exposure
Anti-D is IgG → crosses the placenta

Transfusion — Donor Compatibility

Group	Can donate to	Can receive from
O negative	All — universal donor	O negative only
AB positive	AB positive only	All — universal recipient
A	A, AB	A, O
B	B, AB	B, O

CLINICAL PEARL

Note: "universal donor" applies to packed cells only. Whole O blood still contains anti-A and anti-B in its plasma. Cross-matching is mandatory in every case.

Mismatched Transfusion Reaction

Incompatible RBC transfused → Recipient antibody binds donor RBC → Agglutination + complement activation → Intravascular haemolysis → Free Hb in plasma → haemoglobinuria → Acute tubular necrosis → renal failure

Features

Fever with rigors, loin and chest pain, restlessness
Hypotension and shock
Jaundice, haemoglobinuria (dark urine)
Acute renal failure — the chief cause of death
DIC in severe cases

Erythroblastosis Fetalis (haemolytic Disease of the Newborn)

Rh-negative mother + Rh-positive fetus → Fetal RBC enter maternal circulation at delivery → Mother forms anti-D (IgG) → Next Rh-positive pregnancy → IgG crosses placenta → Haemolysis of fetal RBC

First child usually escapes; risk rises with each pregnancy
Features — anaemia, jaundice within 24 h, hepatosplenomegaly, hydrops fetalis, kernicterus
Prevention — anti-D immunoglobulin 300 µg IM to the mother within 72 hours of delivery, abortion or amniocentesis
Treatment — phototherapy, exchange transfusion, intrauterine transfusion

Other Blood Group Systems and Blood Banking

Other systems — MNS, Lewis, Kell, Duffy, Kidd, Lutheran, P
Stored at 4 °C in CPD-A (citrate-phosphate-dextrose-adenine)
Shelf life 35–42 days
Storage lesion — ↓ 2,3-BPG, ↓ ATP, ↑ K+, ↑ ammonia, ↑ RBC fragility
Component therapy preferred — packed cells, platelets, FFP, cryoprecipitate

Applied Aspects

Cross-matching — major (donor cells + recipient serum) and minor (recipient cells + donor serum)
Coombs test — direct detects antibody already on RBC (newborn); indirect detects free antibody in serum (mother)
Medicolegal — blood groups can exclude but never prove paternity
Massive transfusion complications — citrate toxicity (hypocalcaemia), hyperkalaemia, hypothermia, dilutional coagulopathy
Autologous transfusion — the patient's own blood; avoids all incompatibility and infection risk

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