Blood Groups – UPSC Notes

Blood Groups | UPSC Notes | Legacy IAS Bangalore
GS-III · Science & Technology · Biology · Physiology

Blood & Blood Groups — ABO, Rh Factor & Beyond 🩸

Complete UPSC Notes — Components of blood (plasma, RBC, WBC, platelets), ABO blood group system, Rh factor, transfusion compatibility, blood coagulation, haemolytic disease of the newborn, Bombay blood group (hh), rare blood groups (MAL — 47th system 2024, CRIB — India 2025), and current affairs (National Blood Transfusion Bill 2025).

🅰 Type A: A antigen | Anti-B antibody | Donates to A, AB 🅱 Type B: B antigen | Anti-A antibody | Donates to B, AB 🆎 Type AB: A+B antigens | No antibody | Universal Recipient ⭕ Type O: No antigen | Anti-A + Anti-B | Universal Donor 🇮🇳 CRIB blood group discovered in Bengaluru 2025 | National Blood Transfusion Bill 2025
📚 Legacy IAS — Civil Services Coaching, Bangalore  ·  Updated: April 2026  ·  All Facts Verified
Section 01 — Foundation

🩸 Blood — What Is It & What Does It Contain?

💡 Blood = India's National Highway System

Think of blood as India's national highway network. Plasma is the road itself — the liquid medium that everything travels on. Red Blood Cells (RBCs) are the oxygen tankers — carrying fuel (O₂) from the lungs to every cell and bringing back exhaust (CO₂). White Blood Cells (WBCs) are the police and army — patrolling for foreign invaders (bacteria, viruses) and destroying them. Platelets are the repair crew — rushing to cracks (injuries) and sealing them (clotting) before too much is lost. Remove any one element and the whole transport system collapses. Blood is not just a liquid — it's a living tissue.

🧪 Composition of Blood — At a Glance
🟡 PLASMA — 55%
💧 Water: 90–92%
🔬 Proteins: 6–8% (Fibrinogen, Globulins, Albumins)
🧂 Minerals: Na⁺, Ca²⁺, Mg²⁺, Cl⁻, HCO₃⁻
🍬 Nutrients: Glucose, Amino acids, Lipids
⚙️ Clotting factors (inactive form)
Plasma − clotting factors = Serum
🔴 FORMED ELEMENTS — 45%
🔴 RBC: 5M–5.5M/mm³ | O₂ carrier | 120-day life
WBC: 6,000–8,000/mm³ | Immune defence
🟡 Platelets: 1.5L–3.5L/mm³ | Blood clotting
⚪ WBC Types — Granulocytes & Agranulocytes
Neutrophils 60–65% — Phagocytes; most abundant
Eosinophils 2–3% — Allergy; antiparasitic
Basophils 0.5–1% — Histamine, heparin; least common
Lymphocytes 20–25% — B & T cells; immune response
Monocytes 6–8% — Phagocytes (largest WBC)
Granulocytes: Neutrophils, Eosinophils, Basophils | Agranulocytes: Lymphocytes, Monocytes
📌 Key Blood Facts for UPSC:
• RBCs have NO nucleus in mammals (except camels/llamas — have nucleated RBCs). Biconcave disc shape. Made in red bone marrow. Destroyed in spleen (graveyard of RBCs). Life: 120 days.
Haemoglobin: iron-containing protein in RBC. Carries O₂ (forms oxyhaemoglobin in lungs) and CO₂ (carbaminohaemoglobin from tissues). Normal: 12–17 g/dL (below = anaemia).
Serum = Plasma − Clotting factors. Used in serological tests (ELISA for HIV uses serum).
Fibrinogen (in plasma) → Fibrin (during clotting) via enzyme Thrombin → Thrombin formed from Prothrombin by Thrombokinase complex. Calcium ions (Ca²⁺) are essential for clotting.
Fats are absorbed via lacteals (lymph vessels in intestinal villi) → NOT directly into blood. Lymph carries them.
Section 02 — ABO System

🧬 ABO Blood Group System — Discovered by Karl Landsteiner (1900)

📌 Nobel Prize 1930: Karl Landsteiner won the Nobel Prize in Physiology or Medicine in 1930 for the discovery of human blood groups (ABO system). He also discovered the Rh factor in 1940 along with Alexander Wiener. The ABO system is based on the presence or absence of two antigens (A and B) on the surface of Red Blood Cells and corresponding antibodies (Anti-A and Anti-B) in the plasma. The key principle: your blood contains antibodies against antigens you do NOT have — this triggers immune reactions during incompatible transfusions.
A
🅰 Blood Group A
Antigen: A (on RBC)
Antibody: Anti-B (in plasma)
Gives to: A, AB
Receives from: A, O
B
🅱 Blood Group B
Antigen: B (on RBC)
Antibody: Anti-A (in plasma)
Gives to: B, AB
Receives from: B, O
AB
🆎 Blood Group AB
Antigen: A & B (both)
Antibody: NONE ✅
Gives to: AB only
Receives from: ALL groups
= Universal Recipient
O
⭕ Blood Group O
Antigen: NONE ✅
Antibody: Anti-A & Anti-B
Gives to: ALL groups
Receives from: O only
= Universal Donor
🔄 Blood Transfusion Compatibility Matrix — Donor (column) → Recipient (row)
Recipient ↓ / Donor → A B AB O
A ✓ Yes ✗ No ✗ No ✓ Yes
B ✗ No ✓ Yes ✗ No ✓ Yes
AB (Universal Recipient) ✓ Yes ✓ Yes ✓ Yes ✓ Yes
O (Universal Donor) ✗ No ✗ No ✗ No ✓ Yes

⚠️ "Universal Donor/Recipient" refers to RBC transfusions only. In plasma/whole blood donation, AB is the universal plasma donor (no antibodies), O is the universal plasma recipient.

📌 Why do incompatible transfusions cause reactions? When you receive incompatible blood (e.g., you are Group A receiving Group B blood), your plasma's Anti-B antibodies attack the B antigens on the donated RBCs. This causes agglutination (clumping) → RBCs clump and block blood vessels → haemolysis (RBC rupture) → kidney damage, shock, and can be fatal. This is why cross-matching before transfusion is mandatory.
Section 03 — Rh Factor

🔴 Rh Factor — The Second Critical Blood Group System

📌 Discovery: The Rh (Rhesus) factor was discovered in 1940 by Karl Landsteiner and Alexander Wiener. Named after the Rhesus monkey in which the antigen was first identified. The Rh factor is determined by the presence or absence of the Rh(D) antigen on the surface of RBCs. This creates 8 blood types when combined with ABO: A+, A−, B+, B−, AB+, AB−, O+, O−. Globally: ~85% of people are Rh+ and ~15% are Rh−.
🔴 Rh Positive (Rh+)

Has: Rh(D) antigen on RBC surface.
Antibody: Does NOT naturally have Anti-Rh antibodies. Develops them only after exposure to Rh− blood.
Globally: ~85% of humans are Rh+.
Transfusion: Can receive Rh+ or Rh− blood. Can donate to Rh+ only.
Key: Rh+ person receiving Rh− blood — no problem (Rh− has no Rh antigen, so no reaction).

🔵 Rh Negative (Rh−)

Has: NO Rh(D) antigen on RBC surface.
Antibody: Develops Anti-Rh antibodies after first exposure to Rh+ blood.
Globally: ~15% of humans. Rare in Asia and Africa (<5%), more common in Europeans (~15–17%).
Transfusion: Must receive only Rh− blood. Can donate to Rh+ or Rh−.
O−: Universal donor (no A, B, or Rh antigens — safe for anyone in emergency).

👶 Haemolytic Disease of the Newborn (HDN) / Erythroblastosis Fetalis

🔄 HDN / Erythroblastosis Fetalis — How It Happens
Step 1
First Pregnancy: Rh− mother carries Rh+ baby (inherits Rh+ from father). Usually no problem — fetal and maternal blood don't mix during pregnancy. At delivery, small amounts of Rh+ fetal blood enter mother's circulation.
Step 2
Sensitisation: Mother's immune system recognises Rh+ antigens as foreign → produces Anti-Rh (Anti-D) antibodies. This is called Rh sensitisation. Mother is now "sensitised" — she has IgG Anti-D antibodies that can cross the placenta.
Step 3
Second Pregnancy (Rh+ baby): Mother's Anti-D antibodies cross the placenta and attack the Rh+ RBCs of the fetus → haemolysis (destruction of fetal RBCs) → severe anaemia, jaundice, heart failure in fetus → can be fatal (Erythroblastosis Fetalis).
Prevention
Anti-D immunoglobulin (Rhogam) injection: Given to Rh− mother within 72 hours of delivery of Rh+ baby (or after miscarriage/abortion). Rhogam destroys Rh+ fetal cells in mother's blood before she can form antibodies — prevents sensitisation. Also given at 28 weeks of pregnancy prophylactically.
⚠️ UPSC Trap: HDN affects the SECOND Rh+ baby (not the first). First baby is usually safe. Rh+ mother carrying any baby — NO risk of HDN.
Section 04 — Coagulation

🩹 Blood Coagulation (Clotting) — The Cascade

📌 Why does blood clot? Clotting prevents excessive blood loss after injury. It's a cascade — each step activates the next. Key molecules: Fibrinogen (plasma protein) → Fibrin (insoluble threads that form the clot scaffold). The clot = fibrin network trapping dead cells and platelets = dark reddish-brown scab.
Injury/Trauma → Platelets + Damaged tissue release Thrombokinase (enzyme complex, requires multiple coagulation factors + Ca²⁺)
Thrombokinase converts inactive Prothrombin → active Thrombin
Thrombin converts soluble Fibrinogen → insoluble Fibrin threads
Fibrin threads form a network trapping platelets and RBCs → Blood Clot (Coagulum) — dark reddish-brown scab
🔑 Key Players
  • Ca²⁺ ions: Essential for clotting cascade — anticoagulants (like citrate) work by removing Ca²⁺
  • Vitamin K: Required for synthesis of clotting factors (II, VII, IX, X)
  • Platelets: Release clotting factors on injury
  • Fibrinogen: Plasma protein → converted to Fibrin
  • Thrombin: Key enzyme (from Prothrombin)
🚫 Anticoagulants
  • Heparin: Natural anticoagulant secreted by basophils. Used medically to prevent clotting in surgery, dialysis
  • Warfarin: Oral anticoagulant — inhibits Vitamin K
  • Citrate: Removes Ca²⁺ — used to store blood in blood banks
  • Aspirin: Inhibits platelet aggregation
  • Streptokinase/tPA: Dissolves clots (used in heart attacks — "clot busters")
🩺 Clotting Disorders
  • Haemophilia: X-linked recessive. Deficiency of clotting factor VIII (Haemophilia A — most common) or IX (Haemophilia B — Christmas disease). Affected males cannot form normal clots
  • Thrombosis: Clot inside blood vessel → blocks blood flow. DVT (Deep Vein Thrombosis), Pulmonary Embolism
  • Thrombocytopenia: Low platelet count — dengue causes this
  • DIC: Disseminated Intravascular Coagulation
Section 05 — Rare Blood Groups

🔬 Rare & Special Blood Groups — Beyond ABO

📌 How many blood group systems exist? As of 2025, the International Society of Blood Transfusion (ISBT) recognises 47 blood group systems (after MAL system discovered in 2024). The ABO and Rh systems are the most clinically important. Others include Kell, Duffy, Kidd, Lewis, MNS, Lutheran, and many more. Each system is based on different antigens on RBC surfaces.
🔮 Bombay Blood Group (hh / Oh)

Discovery: First discovered in Bombay (Mumbai), India in 1952 by Dr. Y.M. Bhende.

What makes it special: These individuals lack the H antigen — the precursor on which A and B antigens are built. Without H antigen, even if a person has genes for A or B, they cannot express them.

Key fact: O blood group has H antigen (just no A or B built on top). Bombay group has NO H antigen at all — so they react against ALL ABO groups including O.

Antibodies: Anti-A + Anti-B + Anti-H — incompatible with EVERY known ABO type. Can only receive blood from another Bombay group person.

Prevalence: ~1 in 10,000 in Mumbai; ~1 in 1,000 in certain communities; 1 in 1 million globally.

India 2025: Jaslok Hospital, Mumbai — India's first successful Bombay blood group kidney transplant (Feb 2025). SBTC creating national Bombay group donor registry (2024). Highest prevalence: Maharashtra, Gujarat, Tamil Nadu, Odisha.

🆕 Recently Discovered Blood Group Systems

MAL Blood Group System (2024) — 47th system:
Discovered by NHS Blood and Transplant (NHSBT) and University of Bristol. Solved a 50-year mystery about the AnWj antigen (first found 1972). MAL protein carries the AnWj antigen. Helps ~400 rare-match patients globally per year. Enables precise genotyping for AnWj-negative individuals.

Er Blood Group System (2022):
Based on variants of PIEZO1 protein — critical ion channel in RBCs. Includes 5 antigens: Er1, Er2, Er3, Er4, Er5.

FORS Blood Group System:
Based on Forssman antigen (FORS1). Rare; based on GBGT1 gene.

Langereis (Lan) & Junior (Jr):
Lan-negative and Jr-negative individuals are rare — primarily found in certain ethnic populations. Require specialised screening before transfusion.

Vel Blood Group:
Vel-negative individuals (rare) at high risk of severe transfusion reactions.

June 2025 — 🇮🇳 INDIA (Bengaluru) CRIB Blood Group — India Discovers World's Rarest Blood Type
🔬 Discovery:Scientists from India and the UK identified the world's rarest blood group — named CRIB — in a 38-year-old woman from Kolar, near Bengaluru. The woman was undergoing treatment at Manipal Hospital, Bengaluru, and her blood was found to be incompatible with all 20 tested family members and all known donor samples (panreactivity).
🔤 Name origin:CR = Cromer blood group system (it belongs to). IB = India + Bengaluru (where the case was identified). CRIB is part of the Cromer blood group system — defined by absence of a high-prevalence antigen found in nearly all humans.
📣 Announcement:Discovery officially announced at the 35th Regional Congress of ISBT (International Society of Blood Transfusion) held in Milan, Italy, in June 2025. After 10 months of molecular testing and international research.
🏥 Follow-up:Rotary Bangalore TTK Blood Centre launched a Rare Donor Registry in collaboration with Karnataka State Blood Transfusion Council and ICMR's Indian Institute of Immunohematology (IIH), Mumbai — to provide correct blood to rare blood group patients.
📚 UPSC angle:CRIB blood group; Cromer blood group system; ISBT; ICMR-IIH Mumbai; rare blood group registry; panreactivity; Manipal Hospital Bengaluru; transfusion medicine advancements in India.
Section 06 — Current Affairs

📰 Current Affairs 2024–2026 (Fact-Verified)

Dec 2025 — 🇮🇳 PARLIAMENT National Blood Transfusion Bill, 2025 — India's Dedicated Blood Law
📜 Background:Blood transfusion services in India were previously regulated under dispersed provisions of the Drugs and Cosmetics Act, 1940 — leading to regulatory gaps, inconsistent standards, and varying quality across states. Six thalassaemic children in MP's Satna district contracting HIV through contaminated blood highlighted the urgent need for a dedicated law.
🏛️ Bill introduced:The National Blood Transfusion Bill, 2025 was introduced in Parliament (December 2025) — India's first dedicated legislation for blood transfusion services.
🔑 Key provisions: (1) National Blood Transfusion Authority (NBTA) — new statutory body headquartered in New Delhi, headed by Secretary/Additional Secretary of MoHFW. Chaired by DGHS (Director General of Health Services).
(2) Mandatory registration of all blood centres (existing ones deemed registered for 1 year; registration valid for 5 years).
(3) Uniform national standards for collection, testing, processing, storage, distribution, and transfusion.
(4) National Haemovigilance Programme — tracking adverse reactions from transfusions.
(5) Voluntary non-remunerated donation promoted to ensure safe, ethical blood supply.
(6) Strict penal provisions for violations.
⚠️ Problems addressed:Fragmented legal framework; no uniform standards; urban-rural inequity; seasonal blood shortages; lack of haemovigilance; illegal/unregulated blood banks.
📚 UPSC angle:National Blood Transfusion Bill 2025; NBTA; Haemovigilance; voluntary blood donation; Drugs and Cosmetics Act 1940; thalassaemia; HIV transmission through blood; blood safety legislation.
2024 — 🌍 GLOBAL MAL Blood Group System — 47th Blood Group System Discovered
🔬 Discovery:NHS Blood and Transplant (NHSBT) and University of Bristol identified the MAL (My Antigen London) blood group system — the 47th officially recognised blood group system — solving a mystery dating back to 1972 when the AnWj antigen was first described.
🧬 Science:The MAL protein (a lipid raft-associated protein) was found to carry the AnWj antigen. MAL contains M and N antigens linked to glycophorin A protein. AnWj-negative individuals are very rare but can suffer severe transfusion reactions when receiving blood with the AnWj antigen.
💊 Significance:Helps ~400 rare-match patients globally each year. Enables precise genotyping tests to identify AnWj-negative individuals. Improves transfusion safety for rare blood type patients. As of 2025, there are 47 recognised blood group systems — the ISBT maintains the official registry.
📚 UPSC angle:MAL blood group; 47th blood group system; NHSBT; University of Bristol; AnWj antigen; ISBT; transfusion medicine; personalised medicine; rare blood compatibility.
2024–2025 — 🇮🇳 INDIA Bombay Blood Group — National Registry & India's First Kidney Transplant
📋 Registry:State Blood Transfusion Council (SBTC) initiative: creating national registry for rare Bombay (Oh) blood group donors. Announced 2024. Maharashtra, Gujarat, Tamil Nadu have highest prevalence of Bombay group in India.
🏥 Transplants:India's first successful Bombay blood group kidney transplant performed at Jaslok Hospital, Mumbai, in February 2025. Chennai doctors at MIOT International also performed a cross-blood kidney transplant using plasmapheresis technique (removing antibodies) in mid-2024 for a rare blood group patient.
⚕️ Challenge:Bombay blood group patients cannot receive blood from any ABO group (including O). Blood banks preserve frozen Bombay blood units and maintain donor registries. When compatible blood unavailable: autologous transfusion, cell salvage, or acute normovolemic haemodilution.
📚 UPSC angle:Bombay blood group (hh phenotype); H antigen; anti-H antibody; SBTC; rare donor registry; plasmapheresis; Jaslok Hospital; organ transplantation challenges; blood group compatibility.
Section 07 — Blood Type & Disease

🏥 Blood Groups & Disease Risk — Science-Backed Links

Blood GroupHigher Risk ofLower Risk / ProtectionNotes
AGastric cancer, Pancreatic cancer, Heart disease (higher clotting factors), Smallpox (historically)Higher vWF (von Willebrand factor) and Factor VIII — increased clotting tendency
BHeart disease, Venous thromboembolismNon-O groups have higher vWF and Factor VIII levels
ABCognitive decline, Venous thromboembolism, Autoimmune diseases (immune complexity)Highest level of clotting factors among ABO groups
OPeptic ulcer (H. pylori infections — more H antigen), Bleeding (lower clotting factors — lower vWF)Coronary artery disease, Severe malaria complications, Venous thromboembolismO blood has protective effect against rosetting of Plasmodium falciparum-infected RBCs
Rh−HDN (haemolytic disease of newborn) risk if sensitisedMore common in Europeans (~15%); rare in Asians (<1%); Rh− is NOT a disease
📌 Blood groups and malaria — UPSC important: Blood group O provides protection against severe Plasmodium falciparum malaria because Pf-infected RBCs with group O adhere less to each other and to uninfected cells (rosetting is reduced). Group A blood has more severe malaria complications due to stronger rosetting. This explains why blood group O may have been naturally selected in malaria-endemic regions of Africa.
Section 08 — PYQs & MCQs

📝 Previous Year Questions & Practice MCQs

PYQ — Prelims 2016 Consider the following statements about blood groups:
1. A person with blood group AB has both A and B antigens on red blood cells and no antibodies in plasma.
2. A person with blood group O has no antigens on RBCs and carries both Anti-A and Anti-B antibodies.
3. Blood group O is called universal donor because O blood has no antigens that could trigger immune reactions in any recipient.
4. A person with blood group AB is called universal donor as their plasma has no antibodies.
a) 1 and 2 only
b) 1, 2 and 4 only
c) 1, 2 and 3 only
d) 1, 2, 3 and 4
Statement 1 ✓ — Type AB has both A and B antigens on RBCs and NO antibodies in plasma (since they have both antigens, their immune system doesn't make antibodies against either — that would be self-destructive). This is why AB is the universal recipient — they have no antibodies to attack donated blood. Statement 2 ✓ — Type O has NO antigens on RBC surface, and carries BOTH Anti-A and Anti-B antibodies in plasma. This means O blood can be donated to anyone (no antigens to trigger immune reaction), but O people can only receive from O (they'd attack A or B antigens with their antibodies). Statement 3 ✓ — This correctly explains WHY O is the universal donor — the donated RBCs carry no A or B antigens, so the recipient's antibodies (whatever they may be) have nothing to attack. Note: "Universal donor" strictly applies to RBC transfusions — O plasma contains anti-A and anti-B antibodies which can cause issues in whole blood donation. Statement 4 ✗ — Critical trap! AB is the UNIVERSAL RECIPIENT — NOT the universal donor. AB plasma is the universal PLASMA donor (since AB plasma has no antibodies), but for RBC donation, AB RBCs have both A and B antigens and can only be given to AB recipients. Answer: (c).
PYQ — Prelims 2017 Which of the following statements about the Rh factor is/are correct?
1. The Rh factor was first discovered in Rhesus monkeys.
2. An Rh-negative mother carrying an Rh-positive fetus always has haemolytic disease in the first pregnancy.
3. Anti-D immunoglobulin (Rhogam) is given to prevent Rh sensitisation in Rh-negative mothers.
4. The Rh factor was discovered by Karl Landsteiner and Alexander Wiener in 1940.
a) 1, 2 and 3 only
b) 1, 3 and 4 only
c) 2 and 4 only
d) 1, 2, 3 and 4
Statement 1 ✓ — Rh factor was indeed first identified in Rhesus monkeys (Macaca mulatta). Landsteiner and Wiener injected guinea pigs and rabbits with Rhesus monkey RBCs and found the resulting antibodies also agglutinated 85% of human RBCs — discovering the Rh antigen. Statement 2 ✗ — Key UPSC trap: HDN (Haemolytic Disease of the Newborn) typically does NOT affect the FIRST pregnancy. In the first pregnancy, fetal Rh+ blood enters the mother only at delivery — there's insufficient time to produce enough IgG antibodies to harm the fetus. The mother becomes sensitised after the first delivery. It's the SECOND (or subsequent) Rh+ pregnancies that are at risk — when the already-sensitised mother's anti-D antibodies cross the placenta and attack the fetus. Statement 3 ✓ — Anti-D immunoglobulin (Rhogam/Rh immunoglobulin) works by destroying any Rh+ fetal cells that enter the mother's bloodstream before she can mount an immune response — preventing sensitisation. Given within 72 hours of delivery, miscarriage, or abortion. Also given prophylactically at 28 weeks. Statement 4 ✓ — Karl Landsteiner (who discovered ABO in 1900) and Alexander Wiener discovered the Rh factor in 1940. Landsteiner won the Nobel Prize in 1930 for ABO — ironically before the Rh discovery. Answer: (b).
Q1 Which of the following statements about blood coagulation is/are correct?
1. Calcium ions play an essential role in blood clotting.
2. Fibrinogen is directly converted to fibrin by the enzyme Thrombokinase.
3. Heparin, secreted by basophils, acts as a natural anticoagulant.
4. Vitamin K deficiency can impair blood clotting.
a) 1 and 2 only
b) 1, 3 and 4 only
c) 2, 3 and 4 only
d) 1, 2, 3 and 4
Statement 1 ✓ — Ca²⁺ (calcium ions) are absolutely essential in the coagulation cascade — required for multiple steps. Blood banks use citrate (sodium citrate) to REMOVE calcium from donated blood, preventing it from clotting during storage. Statement 2 ✗ — Trap: Fibrinogen is converted to Fibrin by the enzyme THROMBIN — not Thrombokinase. Thrombokinase is the complex enzyme that converts Prothrombin → Thrombin (the step before). So the sequence is: Thrombokinase converts Prothrombin → Thrombin → Thrombin converts Fibrinogen → Fibrin. A common exam mistake is reversing Thrombin and Thrombokinase. Statement 3 ✓ — Heparin is indeed secreted by basophils (also by mast cells) and is the body's natural anticoagulant — it inhibits thrombin and other clotting factors. Medically, heparin is used to prevent blood clots during surgery, dialysis, and in DVT treatment. Statement 4 ✓ — Vitamin K is essential for the synthesis of clotting factors II (Prothrombin), VII, IX, and X in the liver. Vitamin K deficiency → cannot make these factors → prolonged bleeding. This is why warfarin (an anticoagulant drug) works by inhibiting Vitamin K — it blocks clotting factor synthesis. Newborns are given Vitamin K injection at birth because they lack gut bacteria that produce Vitamin K. Answer: (b).
Q2 The Bombay blood group (hh/Oh phenotype) differs from O blood group because:
1. Bombay group lacks the H antigen which is present in O blood group.
2. O blood group can receive blood from Bombay group donors.
3. Bombay group individuals have Anti-A, Anti-B, and Anti-H antibodies.
4. Bombay group was first discovered in Mumbai, India, in 1952.
a) 1 and 2 only
b) 1, 3 and 4 only
c) 2, 3 and 4 only
d) 1, 2, 3 and 4
Statement 1 ✓ — The crucial distinction: O blood group has the H antigen on RBCs (H antigen is the base on which A and B antigens are built — O group just doesn't add A or B on top of H). Bombay (hh) blood group lacks even the H antigen — this is the fundamental difference. A gene called the H gene (FUT1) is responsible for H antigen production; Bombay group has a rare mutation in both copies of this gene. Statement 2 ✗ — Important reversal trap: O blood group CANNOT receive from Bombay group. Actually it's the reverse: Bombay group individuals CAN donate blood to O group (their blood has no A, B, or H antigens — no antigens means no triggers for immune reactions in the recipient). But O blood group CANNOT be given to Bombay individuals because O blood has H antigens — and Bombay people have anti-H antibodies that will attack H antigens. Bombay individuals can only RECEIVE from other Bombay individuals. Statement 3 ✓ — Bombay group individuals produce Anti-A + Anti-B + Anti-H antibodies — making them incompatible with every known ABO blood type (including O, which has H antigen). Statement 4 ✓ — The Bombay phenotype was first discovered in Bombay (now Mumbai) by Dr. Y.M. Bhende in 1952. Answer: (b).
Q3 With reference to recent developments in blood group science, which of the following is correct?
a) The MAL blood group is the 46th blood group system, discovered to explain the Vel antigen
b) The MAL blood group is the 47th blood group system, solving the mystery of the AnWj antigen first found in 1972
c) CRIB blood group was discovered in Chennai and belongs to the Lewis blood group system
d) The National Blood Transfusion Bill 2025 replaces the Blood Transfusion Act of 1999
Option (b) is correct. The MAL blood group system was identified as the 47th officially recognised blood group system by the ISBT (International Society of Blood Transfusion). Discovered by NHS Blood and Transplant (NHSBT) and University of Bristol. It solved the mystery of the AnWj antigen, which had puzzled researchers since 1972 when it was first described. The MAL protein (lipid raft-associated) carries the AnWj antigen. This discovery helps ~400 rare-match patients globally each year with better compatibility testing. Option (a) is wrong — it's the 47th system (not 46th) and it explains the AnWj antigen (not Vel). Option (c) is wrong — CRIB was discovered in Bengaluru (Kolar), Karnataka — NOT Chennai. It belongs to the Cromer blood group system (CR = Cromer, IB = India-Bengaluru). Announced at ISBT conference in Milan, June 2025. Option (d) is wrong — the National Blood Transfusion Bill 2025 replaces regulatory provisions under the Drugs and Cosmetics Act, 1940 — there was no specific Blood Transfusion Act of 1999. Answer: (b).
Section 09

🧠 Memory Aid — Lock These In

🔑 Blood Groups — All Critical Facts for UPSC

ABO BASICS
A: A antigen + Anti-B antibody | B: B antigen + Anti-A | AB: A+B antigens + NO antibody = Universal Recipient | O: No antigen + Anti-A + Anti-B = Universal Donor. Karl Landsteiner 1900. Nobel Prize 1930.
RH FACTOR
Discovered 1940 by Landsteiner + Wiener. Named after Rhesus monkey. Rh(D) antigen = Rh+. ~85% population Rh+. O− = Universal Donor (no A, B, or Rh antigens). AB+ = Universal Recipient (no antibodies to A, B, or Rh).
HDN / ERF
Erythroblastosis Fetalis / HDN: Rh− mother + Rh+ baby → sensitisation at 1st delivery → Anti-D antibodies → attacks 2ND Rh+ baby. First pregnancy usually SAFE. Prevention: Rhogam (Anti-D immunoglobulin) within 72 hrs of delivery. TRAP: HDN affects 2nd pregnancy, NOT 1st.
COAGULATION
Injury → Platelets release Thrombokinase → Prothrombin → THROMBIN → Fibrinogen → FIBRIN (clot). Ca²⁺ essential. Vitamin K needed for factors II, VII, IX, X. Heparin (basophils) = natural anticoagulant. Serum = Plasma − clotting factors. TRAP: Thrombokinase converts Prothrombin→Thrombin (NOT Fibrinogen→Fibrin).
BOMBAY GROUP
hh / Oh phenotype. Discovered Mumbai 1952 by Dr. Y.M. Bhende. Lacks H antigen (O group has H antigen — key difference). Has Anti-A + Anti-B + Anti-H. Incompatible with ALL ABO groups including O. ONLY can receive from another Bombay group person. Prevalence: 1/10,000 in Mumbai; 1/1M globally. Highest in Maharashtra, Gujarat.
RARE GROUPS
MAL (47th blood group system, 2024) — UK, solved AnWj antigen mystery (1972). CRIB (2025, Bengaluru) — Cromer system, rarest ever, discovered in Kolar woman, ISBT Milan June 2025, Rare Donor Registry launched by Rotary Bangalore TTK. Er system (2022) — PIEZO1 protein. 47 total blood group systems (ISBT).
CURRENT AFFS
National Blood Transfusion Bill 2025 — Parliament Dec 2025, replaces Drugs & Cosmetics Act 1940, creates NBTA (National Blood Transfusion Authority), mandatory registration, haemovigilance programme, voluntary donation. Bombay group national registry (SBTC 2024). India's first Bombay group kidney transplant (Jaslok Hospital Mumbai, Feb 2025).
TRAPS 🪤
• AB = Universal Recipient (NOT donor). • O = Universal Donor (for RBCs). • AB plasma = Universal plasma donor. • HDN: 1st pregnancy SAFE; 2nd at risk. • Bombay group ≠ O group (Bombay lacks H antigen; O has H). • Thrombin converts Fibrinogen→Fibrin (not Thrombokinase). • RBCs have no nucleus in mammals (camels = exception). • Spleen = graveyard of RBCs.
Section 10

❓ FAQs — Concept Clarity

Why is O negative called "universal donor" but O negative people can only receive from O negative?
This is one of the most commonly confused facts about blood groups. The key is understanding the difference between DONATING and RECEIVING. When O− people DONATE: Their RBCs have no A antigen, no B antigen, and no Rh(D) antigen. When transfused into any recipient — whether A+, B−, AB+, O− — the recipient's immune system finds nothing to attack on the donated RBCs. Hence O− is the "universal donor" for RED BLOOD CELL transfusions. When O− people RECEIVE: Their plasma has Anti-A AND Anti-B AND Anti-Rh antibodies. If you give them A+ blood, for example, their Anti-A antibodies attack the A antigens on the donated RBCs → haemolytic reaction. They can only receive blood from O− (which has none of these antigens). This asymmetry is the core of transfusion medicine — the donor's RBCs must be compatible with the RECIPIENT's antibodies. Important nuance: "Universal donor" strictly applies to RBC transfusions. O− whole blood (which contains plasma with Anti-A and Anti-B antibodies) can be problematic in large transfusions because the Anti-A and Anti-B antibodies could attack the recipient's RBCs. This is why modern transfusion medicine mostly uses component therapy (packed RBCs, fresh frozen plasma, platelets separately). For UPSC: Memorise — O− donates to all (no antigens on RBCs) but receives from O− only (has antibodies against A, B, Rh). AB+ receives from all (no antibodies in plasma) but donates RBCs to AB+ only (has A, B, and Rh antigens).
What is the difference between antigen and antibody in the context of blood groups?
In blood group science, these two terms have very specific and testable definitions: Antigens (also called agglutinogens in old terminology): Proteins or carbohydrate structures on the SURFACE of Red Blood Cells. They are markers of identity — they tell the immune system "I belong to this person." In ABO, the antigens are glycoproteins (A and B are sugar-linked proteins). The H antigen is the precursor. Rh antigen (D) is a protein. Antibodies (also called agglutinins): Proteins in the PLASMA (liquid part of blood) that recognise and attack foreign antigens. In blood groups, they are "natural antibodies" — you are born with antibodies against whatever antigens you do NOT have on your own RBCs. Type A person has A antigens on RBCs, so develops Anti-B antibodies (not Anti-A — that would destroy their own cells = autoimmune disaster). The rule: You always have antibodies against the antigens you DON'T have. The reaction: When incompatible blood is transfused, antibodies in the recipient's plasma bind to foreign antigens on donated RBCs → form antigen-antibody complexes → agglutination (clumping) → haemolysis (RBC rupture) → haemolytic transfusion reaction. For UPSC pattern: Antigens are on RBCs; antibodies are in plasma. Type AB — both antigens, no antibodies. Type O — no antigens, both antibodies. Always opposite.
What is haemophilia and why is it called the "royal disease"?
Haemophilia is a genetic blood clotting disorder — the body cannot make adequate amounts of specific clotting factors. Haemophilia A (most common — 80% of cases): Deficiency of Clotting Factor VIII. Haemophilia B (Christmas disease): Deficiency of Clotting Factor IX. Both are X-linked recessive disorders — the faulty gene is on the X chromosome. Why mostly males? Males have one X and one Y chromosome (XY). If the single X chromosome carries the haemophilia gene, there's no "backup" — they have haemophilia. Females have two X chromosomes (XX). They need faulty genes on BOTH X chromosomes to have haemophilia. If only one X is affected, the other provides enough Factor VIII/IX — they are "carriers" (pass it to sons) but usually don't have the disease. Why "royal disease"? Queen Victoria of Britain (1819–1901) was a carrier of Haemophilia B. She passed it to several of her children and grandchildren who married into European royal families — spreading the condition across European royalty. Her grandson Alexei Romanov (heir to the Russian throne) had haemophilia — this influenced Russian politics and arguably contributed to the conditions leading to the Russian Revolution (1917). Treatment: Infusions of the missing clotting factor (recombinant Factor VIII or IX). Gene therapy for haemophilia is now available — HEMGENIX (approved 2022 by FDA) — first gene therapy for Haemophilia B. For UPSC: X-linked recessive; males affected; females are carriers; royal disease (Queen Victoria); Factor VIII deficiency (Haemophilia A); Factor IX deficiency (Haemophilia B).
Section 11

🏁 Conclusion — UPSC Synthesis

🩸 From Two Letters (A, B) to 47 Systems — Blood Is More Complex Than We Knew

When Karl Landsteiner published his discovery of the ABO blood group system in 1900, he solved a mystery that had made blood transfusions life-threateningly unpredictable. His Nobel Prize in 1930 marked a turning point in medicine. A century later, we now know there are at least 47 blood group systems, and the discovery of CRIB from a woman in Bengaluru in 2025 — the rarest blood group ever found — reminds us how much still lies undiscovered in human biology. India's contribution to this field is significant: the Bombay blood group (discovered in Mumbai 1952), CRIB (Bengaluru 2025), and now a dedicated National Blood Transfusion Bill (2025) that seeks to bring regulatory order to one of India's most critical public health systems.

📋 Prelims Key Facts
🧬 ABO: Karl Landsteiner 1900 | Nobel 1930
🐒 Rh factor: Landsteiner + Wiener 1940 (Rhesus monkey)
⭕ O = Universal Donor | AB = Universal Recipient
❌ AB = Universal Donor WRONG (it's Recipient)
👶 HDN: 1st pregnancy SAFE; 2nd Rh+ baby at risk
💉 Rhogam = Anti-D immunoglobulin (prevents HDN)
🏚️ Bombay group: hh, no H antigen, found 1952 Mumbai
🆕 MAL = 47th blood group system (2024, UK)
🇮🇳 CRIB = Bengaluru 2025, Cromer system, rarest ever
🏛️ Blood Transfusion Bill 2025: replaces D&C Act 1940
📝 Mains GS-II/III Topics
🏥 Blood transfusion safety: haemovigilance system
🩸 Haemophilia: gene therapy (HEMGENIX 2022)
👶 HDN: maternal-foetal Rh incompatibility; Rhogam
🔬 Rare blood groups: CRIB, Bombay, MAL — India role
🏛️ National Blood Transfusion Bill 2025: NBTA, provisions
🧬 Personalised medicine: blood groups and disease risk
🦟 Malaria and blood group O: evolutionary protection
🏥 Blood shortage in India: voluntary donation, rural access

Book a Free Demo Class

April 2026
M T W T F S S
 12345
6789101112
13141516171819
20212223242526
27282930  
Categories

Get free Counselling and ₹25,000 Discount

Fill the form – Our experts will call you within 30 mins.