Blood groups &

Blood transfusion

Dr. Smrithi Shetty C.

Professor & Head
Dept of Physiology
AJIMS & RC
PY2.10 Describe different blood groups and
discuss the clinical importance of blood
grouping, blood banking andTransfusion

SLO
• List the blood group systems. Describe the
ABO system, Rh system State the
Landsteiner’s Law
• Describe the mode of inheritance of blood
groups
• Discuss the importance of blood groups
• Discuss the importance and the methods of
cross matching: direct and indirect
• List the physiological basis of the symptoms
and treatment of Rh incompatibility
(erythroblastosis fetalis)
• List the hazards of blood transfusion
• Describe the complications of mismatched
blood transfusion
• Describe how blood is stored and discuss
the changes that occur in stored blood
• Agglutinogens – antigens present on the cell
membranes of RBC.

• Agglutinins- antibodies against the

agglutinogens, present in the plasma

• Agglutination – clumping of RBC-

agglutinogen –agglutinin reaction

( The agglutinins have 2binding sites (IgG) and

10 binding sites (IgM), hence can attach to 2 or
more RBCs at th same time , causing the cells
to clump or agglutinate )
Blood grouping systems
• Depending on the type of Agglutinogen
present or absent on the red cell
membrane

 Major blood group systems

The classical ABO blood grouping system
Rhesus (Rh) blood grouping system

 Minor blood group system

MNS blood group system
P blood group system

 Familial blood group systems

Kell, Duffy,Lutheran,Kidd
The classical ABO blood grouping system

• Based on the presence of agglutinogens A &

B on the RBC membrane
• Agglutinogens A & B – also present in
salivary glands, kidney, liver , pancreas, testis
in body fluids- saliva, semen, amniotic fluid
• Agglutinogens A & B are complex
oligosaccharides
Agglutinins
• Anti-A (α) agglutinin & Anti-B (β) agglutinin
• Reacts with or acts on the Agglutinogens
A&B
(Anti A with Agglutinogen A)
• Anti-A (α) agglutinin & Anti-B (β)
agglutinin- globulins of IgM type ( cannot
cross the placenta)

• Act best at low temperature (5-20oC)- cold

antibodies
ABO blood groups

Blood group Agglutinogen + Agglutinin in

on RBC plasma

A A Anti - B (β )

B B Anti –A (α)

AB A&B NIL

O NIL Anti –A (α) &

Anti - B (β )
3 marks Landsteiner Law
• Karl Landsteiner – 1900

1. If a particular agglutinogen is present on

the RBC membrane of an individual, the
corresponding agglutinin must be absent
in the plasma.

2. If a particular agglutinogen is absent on

the RBC membrane of an individual, the
corresponding agglutinin must be present
in the plasma
• Landsteiner Law is applicable to ABO
blood group system only
• Not applicable to other- Rh , P
- there are no naturally occurring
agglutinins in these systems
Inheritance
• As Mendelian dominant

• 3 genes – A, B & O

• Each persons blood group is determined

by the genes which he/ she receives from
each parent.
Blood group/ Genes from Genotype
Phenotype parents

A A+A AA
A+O AO

B B+B BB
B+O BO

AB A+B AB

O O+O OO
• If blood group of father is B & that of
mother is A, then blood group of the
offspring
Father Mother
Phenotype B A

Genotype BB BO AA AO

offsprings BA, BO, OA, OO

Phenotype AB B A O
• Agglutinogens A & B – develop in 6th
week of fetal life
• At birth conc. is 1/5th of adult level

• Anti-A (α) agglutinin & Anti-B (β)

agglutinin- absent at birth , appear 10-
15days after birth, reach max conc. by the
age of 10yrs.

• What is the mechanism of appearance of

these agglutinins???
• Antigens very similar to A & B antigens are
commonly present in the intestinal bacteria
& foods

• Newborn exposed to these antigens

• Antigens recognized as non-self

• Stimulate the formation of antibodies

against the antigen by the immune system
Determination of blood groups
• Mixing a drop of blood with a drop of anti-
sera
 Anti serum A ( containing α agglutinins)
 Anti serum B (containing β agglutinins)
Separately on a glass slide

• Anti serum A will cause agglutination

(clumping) of RBC having A agglutinogens
• Anti serum B will cause agglutination
(clumping) of RBC having B agglutinogens
Rhesus ( Rh) blood group
• Landsteiner & Weiner -1940
• Based on the presence of Rh antigens- 2
types

• 85 % Rh +ve – have Rh antigens on RBC

membrane & no Rh antibody

• 15% Rh –ve – have no Rh antigens & no

Rh antibody

• Detected only on RBC membrane

• Rh antigens- 3 types : C,D,E
• Most common :D

Rh antibodies- not naturally present

Produced only when:
1. Rh –ve individual is transfused with
Rh+ve blood
2. Rh-ve mother gives birth to Rh+ve baby

Ig G type, can cross the placenta

warm antibodies
Inheritance
• 2 genes: D & d
• D is dominant
• Rh +ve – DD or Dd
• Rh –ve – dd

• If father Rh +ve, mother Rh-ve

DD or Dd dd

Offspring Dd, Dd, Dd, dd

Rh +ve Rh +ve Rh +ve Rh -ve

Exercise
1. Blood group of an individual is B +ve.
Name the agglutinogens and agglutinins
present in his blood

• Agglutinogens on RBC membrane:

B & Rh antigens
• Agglutinins in plasma:
Anti A antibody
1. Blood group of an individual is O +ve.
Name the agglutinogens and agglutinins
present in his blood

• Agglutinogens on RBC membrane:

Rh antigen
• Agglutinins in plasma:
Anti A & Anti B antibodies
1. Blood group of an individual is A -ve.
Name the agglutinogens and agglutinins
present in his blood

• Agglutinogens on RBC membrane:

A antigen
• Agglutinins in plasma:
Anti B antibody
3marks Bombay blood group (hh)
• Discovered 1st by Dr.Y.M.Bhende in
Bombay in 1952
• Rare type of blood group
• Absence of antigen A, B and also antigen
H
 H antigen
• (Agglutinogens / Antigens are complex
oligosaccharides)
• On the RBC membrane, there is precursor
substance
• H gene codes for an enzyme that adds the
sugar Fucose to the terminal sugar of a
precursor substance
RBC precursor
RBC
membrane

Glucose

Galactose

N acetlygalactosamine

Galactose
Formation of H RBC

antigen on
RBC precursor
Glucose
membrane

Galactose

N acetlygalactosamine

Fucose Galactose
• H antigen is the foundation upon which A
and B antigens are built
• The “A” gene codes for an enzyme that
adds N acetlygalactosamine to the
terminal sugar of H antigen
• The “B” gene codes for an enzyme that
adds D galactose to the terminal sugar of
H antigen
 RBC

Formation of A
Glucose
antigen

Galactose

N acetlygalactosamine

Fucose Galactose

N acetlygalactosamine
 RBC

Formation of B
Glucose
antigen

Galactose

N acetlygalactosamine

Fucose Galactose

Galactose
 • Group O individuals have no A and B
antigens, but have H antigen on the RBC
membrane
• Group A individuals have A and H
antigens on the RBC membrane
• Group B individuals have B and H
antigens on the RBC membrane
• B
A
B
A
A B
A
B B
A A
Group o with H Group A with A & H Group B with B & H
antigen sites antigen sites antigen sites
• H antigen is found on RBC when the
person has HH genotype or Hh genotype
but not from hh genotype.
• This type of blood group is Bombay blood
group inherited as hh
Bombay blood group (hh)
• Discovered 1st by Dr.Y.M.Bhende in
Bombay in 1952
• Rare type of blood group
• Absence of antigen A, B and also antigen
H
• Their sera contain anti-A and anti-B and
anti-H.
• People who have Bombay phenotype can
donate RBCs to any member of the ABO
blood group system
• But they can receive only from bombay
blood group
 Haemolytic disease of the
5marks newborn
• Erythroblastosis fetalis is the disease of
the fetus and the newborn child
characrterised by agglutination and
phagocytosis of the fetal red blood cells
• Rh incompatibility between the mother &
fetus.
• Mother Rh-ve , fetus Rh+ve.
Erythroblastosis fetalis
• 1st pregnancy
Mother Fetus
Rh-ve Rh+ve
blood flow

during pregnancy

• Fetal blood doesn’t enter the mothers

circulation
• During delivery of 1st baby
Rh-ve Mother Rh+ve Fetus

mixing of fetal &

maternal blood
during delivery

baby delivered
Rh+ve blood (Rh Ag) enters maternal
circulation

• Sensitizes mother to produce

anti Rh Antibodies
• 2nd pregnancy
Rh-ve Mother Rh+ve Fetus
already anti Rh Ab (IgG)
produced
blood flow
during pregnancy

Anti Rh Ab reacts with Rh +ve

RBC
Crosses the placenta

Agglutination

Haemolytic disease
• Depending on the severity
1. Erythroblastosis fetalis: appearance of
large number of erythroblasts in
circulation—anemia
2. Icterus gravis neonatorum: jaundice,liver
spleen enlarged
3. Kernicterus: bilirubin enters into brain
tissue & damages(basal ganglia)-
neurological manifestations
4. Hydrops fetalis: grossly edematous, severe
hemolysis- intra uterine death
• Treatment
 Exchange transfusion – replacement of baby’s
Rh+ve blood with Rh-ve blood

• Prevention
 Injecting anti Rh Abs (Anti D antibodies) - in
the form of Rh Ig to mother within 72hrs of
delivery

 These Rh Abs destroys Rh+ve RBC which has

entered mothers circulation
Clinical applications of blood
grouping / uses
1. In blood transfusion
2. In prevention of haemolytic disease of
newborn
3. In paternity disputes
4. In medico-legal cases
5. In knowing susceptibility to diseases
eg:
 O blood group- more susceptible for
peptic ulcers
 A- Ca stomach
Blood transfusion
• Indications :

1. Blood loss- accidents, major surgery

2. Severe anemia
3. Exchange transfusion
4. Blood diseases- hemophilia
5. Acute poisoning-CO poisoning
• Donor , universal donor
• Recipient
• Precautions to be taken:
 Donor –healthy, 18-60yrs
 Donor screened for diseases-HIV, hepatitis,
malaria, syphilis
 Cross matching:
Major Cross matching : donor cells mixed with
recipient plasma
Minor : recipient cells with donor plasma
If agglutination occurs-blood should not be
transfused
 Autologous transfusion
5
Hazards of blood transfusion
1. Mismatch transfusion reactions
2. Circulatory overload
3. Transmission of blood borne diseases
4. Pyrogenic reactions
5. Allergic reactions
6. Hyperkalemia
7. Hypocalcemia
8. Haemosiderosis
9. Air embolism
 Mismatch transfusion reactions
5
• Agglutination of donor cells

• Clumps Blocks blood vessels

• Tissue ischaemia

• Severe pain / tightness in chest

 Agglutination of donor RBCs

Haemolysis
( phagocytosis of agglutinated cells)

Haemoglobinemia

Haemolytic
Haemoglobinuria jaundice
Free Hb

Precipitate in tubules

Obstruct tubules

Renal tubular damage

 Haemolysis

Toxic substances released

Renal vasoconstriction

Decrease BP

Circulatory shock
 Renal tubular
Decrease BP Circulatory Renal vaso
damage
shock constriction

Acute renal shut down- anuria

Acute Renal failure

Coma & death

Summary
• ABO and Rh blood group systems
• Clinical application
• Bombay blood group,
Erythroblastosis fetalis
• Blood transfusion, indications
• Hazards of mismatch transfusion
The end