PROF. Vd .

YOGITA SHROTRIYA
 BLOOD GROUP
• AUSTRIAN SCIENTIST KARL LANDSTEINER, IN 1901.
• HE WAS HONOURED WITH NOBEL PRIZE IN 1930 FOR THIS DISCOVERY
• THE RHESUS SYSTEM (Rh SYSTEM) WAS DISCOVERED IN 1940.

• LANDSTEINER LAW STATES THAT:

• 1. IF A PARTICULAR AGGLUTINOGEN (ANTIGEN) IS PRESENT IN THE RBCS,
CORRESPONDING AGGLUTININ (ANTIBODY) MUST BE ABSENT IN THE SERUM.
• 2. IF A PARTICULAR AGGLUTINOGEN IS ABSENT IN THE RBCS , THE CORRESPONDING
AGGLUTININ MUST BE PRESENT IN THE SERUM.

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 BLOOD GROUP
• THERE ARE AT LEAST 24 BLOOD GROUPS AND MORE THAN 100 ANTIGENS THAT CAN BE
DETECTED ON THE SURFACE OF RED BLOOD CELLS. HERE WE DISCUSS TWO MAJOR
BLOOD GROUPS—ABO AND RH.
• THE ABO BLOOD GROUP IS BASED ON TWO GLYCOLIPID ANTIGENS CALLED A AND B .
• PEOPLE WHOSE RBCS DISPLAY ONLY ANTIGEN A HAVE TYPE A BLOOD.
• THOSE WHO HAVE ONLY ANTIGEN B ARE TYPE B.
• INDIVIDUALS WHO HAVE BOTH A AND B ANTIGENS ARE TYPE AB;
• THOSE WHO HAVE NEITHER ANTIGEN A NOR B ARE TYPE O.
• BLOOD PLASMA USUALLY CONTAINS ANTIBODIES CALLED AGGLUTININS THAT REACT
WITH THE A OR B ANTIGENS IF THE TWO ARE MIXED.
• THESE ARE THE ANTI-A ANTIBODY, WHICH REACTS WITH ANTIGEN A, AND THE ANTI-B
ANTIBODY, WHICH REACTS WITH ANTIGEN B.
• OTHER BLOOD GROUPS-
• AUBERGER GROUPS ,P GROUP, KELL GROUP, I GROUP, KIDD GROUP, SULTER XG GROUP,
DIEGO GROUP, BOMBAY GROUP, DUFFY GROUP, LUTHERAN GR
• MNS BLOOD GROUPS ARE DETERMINED BY THEIR REACTIONS WITH ANTI-M, ANTI-N
AND ANTI-S. HOWEVER, THESE BLOOD GROUPS RARELY CAUSE ANY TROUBLE LIKE
HEMOLYSIS FOLLOWING TRANSFUSION.

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PHYSIOLOGICAL BASIS OF BLOOD GROUP

THE PHENOMENON OF HAEMOAGGLUTINATION IS DUE TO THE INTERACTION BETWEEN TWO FACTORS –

AGGLUTINOGENS, PRESENT IN THE CORPUSCLES AND AGGLUTININS, PRESENT IN THE PLASMA (OR
SERUM).
THE AGGLUTINOGENS ARE INHERITED AS MENDELIAN DOMINANTS.
THE CORPUSCLES OF A PARTICULAR SUBJECT MAY CONTAIN ONLY A OR ONLY B OR BOTH A AND B OR NO
AGGLUTINOGENS AT ALL, i.e. O.
SIMILARLY, THE SERUM MAY CONTAIN ONLY A OR ONLY B OR BOTH A AND B OR NO AGGLUTININS.
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 BLOOD GROUP TYPES
• THE BLOOD GROUPS ARE MAINLY OF THREE TYPES
• 1. A, B AND O GROUPS
• 2. Rh FACTOR
• 3. M AND N FACTORS
• SOME OTHER BLOOD GROUP CHARACTERISTICS ( i.e. P, LUTHERAN, LEWIS AND
OTHERS) EXCEPTING THE ABOVE THREE ARE ALSO PRESENT.
• A,B AND O BLOOD GROUPS
• THE PHENOMENON OF HAEMOAGGLUTINATION IS DUE TO THE INTERACTION
BETWEEN TWO FACTORS –AGGLUTINOGENS , PRESENT IN THE CORPUSCLES
AND AGGLUTININS, PRESENT IN THE PLASMA (OR SERUM).
• THERE ARE TWO PRIMARY AGGLUTINOGENS-A AND B;
• THERE ARE TWO CORRESPONDING AGGLUTININS -alfa AND beta.
• THE AGGLUTINOGENS ARE INHERITED AS MENDELIAN DOMINANTS.
• THE CORPUSCLES OF A PARTICULAR SUBJECT MAY CONTAIN ONLY A OR ONLY B
OR BOTH A AND B OR NO AGGLUTINOGENS AT ALL, I.E. O. SIMILARLY, THE
SERUM MAY CONTAIN ONLY alfa OR ONLY beta OR BOTH alfa AND beta OR NO
AGGLUTININS.

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PHYSIOLOGICAL BASIS OF BLOOD GROUP

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PHYSIOLOGICAL BASIS OF BLOOD GROUP

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 AGGLUTINOGENS
• 1.AGGLUTINOGENS START APPEARING IN THE SIXTH WEEK OF FOETAL LIFE.
CONCENTRATION GRADUALLY RISES AND AT BIRTH IT REACHES ONE-FOURTH OF
THE ADULT LEVEL. THE ADULT LEVEL IS REACHED AT ABOUT PUBERTY.
• 2. AGGLUTINOGENS A AND B, ARE POLYSACCHARIDES. THEY ARE NOT ONLY
FOUND IN RED CELLS BUT IN THE CELLS OF MANY OTHER ORGANS, SUCH AS
SALIVARY GLANDS, PANCREAS, LIVER, LUNGS, TESTES, ETC. THEY ARE SOLUBLE
IN WATER AND AS SUCH DIFFUSE OUT INTO THE BODY FLUIDS.
• 3. THUS, HUMAN BEINGS MAY BE OUT INTO FOUR GROUPS ACCORDING TO THE
NATURE OF THE AGGLUTINOGENS POSSESSED BY THEIR CORPUSCLES. THESE
GROUPS ARE CALLED O, A, B, AND AB.

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 AGGLUTININS
• 1.THE SPECIFIC AGGLUTININS ARE NOT PRESENT IN THE FOETAL PLASMA. BUT
MATERNAL AGGLUTININS, BEING FILTERED THROUGH THE PLACENTA, ARE
FOUND IN THE FOETAL PLASMA. ONLY 50% OF NEWBORN INFANTS SHOW AN
APPRECIABLE AMOUNT OF THIS AGGLUTININ.
• 2. SPECIFIC AGGLUTININS START APPEARING FROM ABOUT THE 10TH DAY
AFTER BIRTH AND RISES TO THE MAXIMUM AT ABOUT THE 10TH YEAR.
• 3. AGGLUTININS, LIKE OTHER ANTIBODIES, ARE FOUND IN THE GLOBULIN
FRACTION OF THE SERUM.
• 4. THEY ARE ALSO PRESENT IN LOW DILUTIONS IN BODY FLUIDS WHICH ARE
RICH IN PROTEINS, SUCH AS MILK, LYMPH EXUDATES AND TRANSUDATES.
THEY ARE NOT FOUND IN URINE AND CEREBROSPINAL FLUID.
• 5. HAEMOAGGLUTININS INCREASE TEMPORARILY DURING SERUM SICKNESS
AND ARE REDUCED IN LEUKAEMIA.
• 6. LIKE OTHER ANTIBODIES, THE CONCENTRATION OF SPECIFIC AGGLUTININ
VARIES AT ALL AGES FROM MAN TO MAN AND EVEN IN THE SAME INDIVIDUAL
UNDER DIFFERENT CONDITIONS. THEY ACT BEST AT A LOWER TEMPERATURE.
• 7. THE BLOOD GROUP OF A PARTICULAR SUBJECT IS A FIXED CHARACTER AND
DOES NOT VARY WITH AGE, OR DISEASE.

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 RHESUS FACTOR
• DISCOVERY OF Rh GROUP SYSTEM-
• ANOTHER IMPORTANT AGGLUTINOGENS HAVE BEEN DEMONSTRATED (1940) IN
HUMAN RED CORPUSCLES ALSO BY LANDSTEINER AND WIENER. (KARL LANDSTEINER
1868-1943)
• RBCS OF RHESUS MONKEYS WHEN INJECTED INTO RABBITS ,THE RABBITS RESPONDED
TO THE PRESENCE OF AN ANTIGEN IN THESE CELLS BY FORMING AN ANTIBODY WHICH
AGGLUTINATED RHESUS RBCS.
• AGGLUTINATION OCCURS IN 85% OF MEN ,THESE PEOPLE ARE CALLED Rh + VE.
• NO AGGLUTINATION OCCURS IN 15% ,THESE ARE CALLED – VE AND THEIR SERUM ALSO
CONTAINS NO Rh ANTIBODY.
• IT IS THE AGGLUTINOGENS OF THE RHESUS MONKEY AND IS PRESENT IN 85% OF WHITE
PEOPLE. THERE IS NO CORRESPONDING AGGLUTININ IN THE HUMAN PLASMA.
• Rh AGGLUTINOGENS : THERE ARE SIX OR THREE PAIRS OF Rh AGGLUTINOGENS-C, c; D,
d; AND E, e. C, D AND E ARE MENDELIAN DOMINANTS, WHILE c, d and e ARE
RECESSIVE.

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 IMPORTANCE OF Rh FACTOR
• CLINICAL IMPORTANCE:
• IF Rh +VE BLOOD BE TRANSFUSED TO AN Rh -VE PATIENT, AN ANTI-Rh
FACTOR WILL DEVELOP IN THE PATIENT'S BLOOD IN ABOUT 12 DAYS.
• IF A SECOND TRANSFUSION OF SAME BLOOD BE GIVEN TO SUCH A PATIENT
AFTER THIS PERIOD, HEMAGGLUTINATION OF THE DONOR'S CORPUSCLES
WILL TAKE PLACE.
• IN OTHER WORDS, BLOOD WHICH WAS COMPATIBLE BEFORE HAS BECOME
INCOMPATIBLE NOW.
• SO THAT BEFORE TRANSFUSION THE TEST FOR RH FACTOR SHOULD BE
CAREFULLY DONE.

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 HEMOLYTIC DISEASE OF NEW BORN

• THIS DISEASE IS DUE TO DESTRUCTION OF THE RH +VE RBC IN THE FOETUS BY

AN ANTI-Rh AGGLUTININ, PRESENT IN THE MOTHER'S SERUM, WHICH HAS
FILTERED THROUGH THE PLACENTA DURING PREGNANCY.
• THE INCOMPATIBILITY BETWEEN THE BLOOD OF MOTHER AND CHILD IS CAUSED
BY THE INHERITANCE OF THE RH FACTOR.
• INCOMPATIBILITY OF THE BLOOD MIGHT ARISE ONLY IN CASE MARKED AS RISK
(AS IN THESE TWO GROUPS THE MOTHER IS CAPABLE OF PRODUCING AN ANTI-
Rh AGGLUTININ TO DESTROY THE Rh +VE RBC), PRESENT IN THE FOETUS.
• IN THIS DISEASE, DESTRUCTION OF THE NORMAL RBC LEADS TO THE PRESENCE
OF ABNORMAL NUCLEATED RBC IN CIRCULATION. A FEW HOURS AFTER BIRTH
THERE IS ANAEMIA, ACUTE JAUNDICE AND RELATED SYMPTOMS.

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 ERYTHROBLASTOSIS FETALIS

• ERYTHROBLASTOSIS FETALIS IS A DISORDER IN FETUS, CHARACTERIZED BY THE

PRESENCE OF ERYTHROBLASTS IN BLOOD.
• DURING PREGNANCY THE FOETUS MAY BE Rh +VE WHEREAS THE MOTHER Rh -
VE. THE Rh AGGLUTINOGENS (SLIGHTLY PRESENT ALSO IN THE PLASMA) FROM
THE FOETUS PASS INTO THE MATERNAL BLOOD AND STIMULATES THE
FORMATION OF ANTI-Rh FACTOR. THIS ANTIBODY ENTERS THE FOETAL BLOOD
AND DESTROYS THE RED CELLS OF THE FOETUS. THE FOETUS MAY DIE (CAUSING
MISCARRIAGE) OR IF BORN ALIVE, SUFFERS FROM SEVERE ANAEMIA (
ERYTHROBLASTOSIS FOETALIS).
• SUCH A MOTHER BECOMES SENSITISED TO RH FACTOR. IN FUTURE IF SHE GETS
A TRANSFUSION OF OTHERWISE COMPATIBLE BLOOD BUT CONTAINING Rh
FACTOR, AGGLUTINATION WILL TAKE PLACE.
• FOR THE SAME REASON, A Rh NEGATIVE WOMAN, BEFORE MENOPAUSE
SHOULD NOT BE GIVE TRANSFUSION OF Rh POSITIVE BLOOD. BECAUSE, IN
CASES SHE BECOMES PREGNANT WITH Rh POSITIVE FOETUS, IT CAN BE A
PROBLEM .

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 CLINICAL IMPORTANCE OF BLOOD GROUP

• INDIVIDUALS HAVE DIFFERENT TYPES OF ANTIGEN ON THE SURFACES OF THEIR RED BLOOD
CELLS. THESE ANTIGENS, WHICH ARE INHERITED, DETERMINE THE INDIVIDUAL'S BLOOD GROUP.
• RBCS CARRY THE BLOOD GROUP ANTIGENS LIKE A ANTIGEN, B ANTIGEN AND RH FACTOR. THIS
HELPS IN DETERMINATION OF BLOOD GROUP AND ENABLES TO PREVENT REACTIONS DUE TO
INCOMPATIBLE BLOOD TRANSFUSION .
• THE MAIN SIGNS ARE CLUMPING OF RED BLOOD CELLS, HEMOLYSIS, SHOCK AND KIDNEY
FAILURE.
• THESE ANTIBODIES CIRCULATE IN THE BLOODSTREAM AND THE ABILITY TO MAKE THEM, LIKE
THE ANTIGENS, IS GENETICALLY DETERMINED AND NOT ASSOCIATED WITH ACQUIRED
IMMUNITY
• IF INDIVIDUALS ARE TRANSFUSED WITH BLOOD OF THE SAME GROUP, i.e. POSSESSING THE
SAME ANTIGENS ON THE SURFACE OF THE CELLS, THEIR IMMUNE SYSTEM WILL NOT RECOGNIZE
THEM AS FOREIGN AND WILL NOT REJECT THEM.
• HOWEVER, IF THEY ARE GIVEN BLOOD FROM AN INDIVIDUAL OF A DIFFERENT BLOOD TYPE, i.e.
WITH A DIFFERENT TYPE OF ANTIGEN ON THE RED CELLS, THEIR IMMUNE SYSTEM WILL MOUNT
AN ATTACK UPON THEM AND DESTROY THE TRANSFUSED CELLS. THIS IS THE BASIS OF THE
TRANSFUSION REACTION; THE TWO BLOOD TYPES, THE DONOR AND THE RECIPIENT, ARE
INCOMPATIBLE.

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DETERMINATION OF BLOOD GROUP

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 IMPORTANCE OF BLOOD GROUP
• 1. BLOOD DONATION

• 2. CERTAIN BLOOD DISEASE

• 3. PATERNITY TEST

• 4. IN FORENSIC MEDICINE

• 5. ETHNOLOGICAL STUDIES – STUDY OF CHARACTERISTICS OF DIFFERENT PEOPLES

AND THE DIFFERENCES & RELATIONSHIPS BETWEEN THEM.

• 6. ANTHROPOLOGICAL STUDIES – STUDY OF HUMAN BIOLOGICAL &

PHYSIOLOGICAL CHARACTERISTICS & THEIR EVOLUTION.

• 7. VARIOUS EXPERIMENTAL PURPOSES

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 CROSS MATCHING

A O

AB B

UNIVERSAL DONOR BLOOD GROUP IS O –VE

UNIVERSAL RECIPIENTS BLOOD GROUP IS AB+ VE
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 INDICATIONS FOR BLOOD TRANSFUSION

• 1. HAEMORRHAGE EITHER ACUTE OR CHRONIC (ESPECIALLY IF THE HAEMOGLOBIN

FALLS BELOW 40%).
• 2. SHOCK IN ORDER TO INCREASE THE BLOOD VOLUME.
• 3. BLOOD DISEASES, e.g. IN ALL VARIETIES OF SEVERE ANAEMIA WHERE THE
HAEMOGLOBIN IS BELOW 40% APLASTIC ANAEMIA, HAEMORRHAGIC DISEASES OF THE
NEWBORN,HAEMOPHILIA, PURPURA HAEMORRHAGICA, etc.
• IN HAEMORRHAGIC DISEASES BLOOD TRANSFUSION INCREASES COAGULABILITY.
• 4. IN CARBON MONOXIDE POISONING, COAL GAS POISONING etc. WHERE
HAEMOGLOBIN HAS FORMED SOME OTHER ABNORMAL COMPOUNDS, BLOOD
TRANSFUSION PROVIDES A FRESH SUPPLY OF OXYHAEMOGLOBIN.

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 HAZARDS OF INCOMPATIBLE BLOOD TRANSFUSION

• 1. AGGLUTINATION OF RED CELLS & HEMOLYSIS

• 2. JAUNDICE
• 3. HEMOGLOBINUREA
• 4. RENAL FAILURE
• 5. FEBRILE REACTIONS – FEVER , RIGOR
• 6. ALLERGIC REACTIONS - ITCHING , URTICARIA , ERYTHEMA
• 7. TRANSMISSION OF DISEASES - HEPATITIS , MALARIA , AIDS , SYPHILIS
• 8. CIRCULATORY OVERLOAD- HEART FAILURE , PULMONARY EDEMA
• 9. THRMBOPHLEBITIS , AIR EMBOLISM DUE TO FAULTY TECHNIQUE OF
TRANSMISSION .

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