Blood Groups and abo grouping and RH system

mbbs

2. USES OF BLOOD GROUP TESTING
•In blood transfusion
•In pregnancy
•Investigating paternal dispute
•Medico legal value
•Anthropological purposes
•For matching tissues during organ
transplantation

3. DISCOVERY OF BLOOD GROUPS
1901 Karl Landsteiner ABO system
1927
Karl Landsteiner
Philip Levine
M, N and MN
system
1940
Karl Landsteiner
Weiner
Rh factor

4. DISTRIBUTION OF ABO GROUPS
“A”
21%
(A1 -75% A2 -25%)
“B” 39%
“AB” 9%
“O” 31%

5. http://learn.genetics.utah.edu/units/basics/blood/types.cfm

6. Blood Types

7. Chemical nature of the antigen
•The principal nature of the antigen is –
mucopolysaccharides
•Molecular weight –2,00,000 –3,00,000
•The specificity of the antigenic reaction
is dependent on the carbohydrate
moiety
•Antigenic substance of blood group
antigens are present in saliva, salivary
secretion and ovarian cyst fluid

9. BLOOD GROUPS
•Antigen –AGGLUTINOGEN
ISOHEMAGGLUTINOGEN
•Antibodies –AGGLUTININ
ISOHEMAGGLUTININ

10. BLOOD GROUPS
BLOOD
GROUP
ANTIGEN
(Agglutinogen)
ANTIBODY
(Agglutinin)
“A” A Anti -B
“B” B Anti -A
“AB” A and B Nil
“O” Nil
Anti –A and
Anti -B

12. LANDSTEINER’S LAW
•FIRST LAW
•If an agglutinogenis present on the red cell
of an individual the corresponding
agglutininmust be absent from the plasma
•SECOND LAW
•If an agglutinogenis absent on the red cell
of an individual the corresponding
agglutininmust be present in the plasma

13. Rh BLOOD GROUP
•LANDSTEINER and WEINER found this in
RHESUS MONKEY (Macaca mulatta)
•Named after it as Rh antigen
•Rh antigen when injected into rabbit produced
antibodieswhich agglutinated rhesus red cells
as well as human red cells
•85% of individuals Rh + ve
•15% Rh –ve

14. Rh BLOOD GROUP
•99% of Indians are Rh + ve
•Rh antigen is not found in tissues and secretions
•The locus for Rh gene is chromosome 1
•Several varieties of Rh Antigen (C,D,E,c,d and e)
•‘C,E,c’ and ‘e’ are not very immunogenic and ‘d’
does not produce antibodies
•‘D’ is the most common and most immunogenic

15. Rh blood group
•Rh antibodies are not naturally
occuring antibodies
•Antibodies are produced only
when the person is sensitized
with Rh antigen
•Mismatched blood transfusion
•feto maternal leak occurs during
delivery

16. How to determine blood group
•By mixing a drop of isotonic saline
suspension of subject’s RBC’s
with a drop of anti A serum, anti B
serum, anti Rh serumseparately
on a porcelain tile or glass slide
•See whether agglutination occurs
or not

17. D

18. How to determine blood group
PROCEDURE:
1.Divide the porcelain tile into four columns with a
markingpencil.
2.Mark the columns as A, B, Rh andcontrol.
3.Take 1ml of normal saline in a testtube.
4.Prick the finger with the lancet under aseptic
conditions.
5.Mix 3-5 drops of blood with the saline to obtain a
suspension of red bloodcells.
6.Add a drop each of anti-A, anti-B, anti-D sera and
saline to the respectivecolumns.

19. How to determine blood group
PROCEDURE: (contd)
Place a drop of the red cell suspension adjacent to the
anti-sera in the respectivecolumns.
Mix the anti-sera and red cell suspension by using
separate sticks for eachcolumn.
Wait for few minutes and observe the agglutination.
Compare it with the salinestandard.
Record yourfindings.
If there is doubt regarding agglutination, confirm it
undermicroscope.

20. Blood grouping

22. AGGLUTINATION OF
RBC’s

24. DETERMINATION OF BLOOD GROUPING & TYPING
AIM: To determine the ABO blood group and Rh type of the given
blood sample.
APPARATUS REQUIRED: Lancet, spirit, cotton, normal saline,
clean white porcelain tile, glass marking pencil, anti-A serum, anti-B
serum, anti-D serum, small sticks for mixing, glass slides, microscope.
PRINCIPLE: Determination of blood groups is done by using
specific agglutinins (antibodies) to confirm the presence or absence of
corresponding agglutinogens (antigens) on the surface of the red blood
cells.
RESULT:
The blood group and Rh typing of the subject is .......................

25. OTHER BLOOD GROUPS
•M group
•N group
•MN group
•P group
•LUTHERAN
•KELL
•LEWIS
•DUFFY

26. •A and B antigens also
will not be produced
•The result is an O
phenotype by default
since a lack of A and B
antigens is the O type
•Antibodies produced
will agglutinate A & B
and H antigens

27. Bombay blood group
•Discovered in 1952 by Dr.Y.M.Bhende
in Bombay in certain group of ‘Marathi’
speaking individuals
•Their genotype is hhand Phenotype is O
•They do not inherit an H Antigen from
either parent
•A or B antigen are not formed or O is also
possible since H is not there

28. Bombay blood group
•No Antigen -RBCs are not agglutinate by
Anti –A or Anti –B serum
•They have all three ABO antibodies
•So they cannot receive blood from ABO
group persons
•They can receive blood from only the same
type of person

30. Four types :
1.Type I Reaction/anaphylaxis
2.Type II Reaction/Cytotoxic reaction
3.Type III Reaction/ Immune complex
disease
4.Type IV Reaction/cell mediated
reaction/delayed hypersensitivity
reactions
Hypersensitivity Reactions

32. Type I /anaphylaxis
1.Usually occur in Re
exposure
2.Highly sensitive
individuals –first
exposure
3.Ag-Abcomplex –
release histamine &
SRS from mast cells
and basophils
4.Acute hypotension
5.Myocardial contractility
decreases –reduced
CO –acute medical
emergency
Type II /Cytotoxic reaction
•IgG& IgMdirectly acts
against Ag present in
person’s RBC.
•Incompatible blood
transfusion, hemolytic
diseases of newborn,
autoimmune hemolytic
anemia
•Acute hemolysis
•Medical emergency

33. Type III / Immune
complex disease
1.Ag-Abcomplex
escapes phagocytosis
2.Deposited in the
basement membrane
of blood vessels
3.Activates complement
4.Inflammation
1.Glomerulonephriti
s
2.SLE
3.RA
Type IV /cell mediated
reaction/delayed
hypersensitivity reactions
•Macrophage mediated
•Activated by T cells
•Skin test for
tuberculosis

34. •A person with Rh-blood can developRh antibodies
in the blood plasma if he or she receives blood from a
person with Rh+ blood, whose Rh antigens can trigger
the production of Rh antibodies.
•A person with Rh+ blood can receive blood from
a person with Rh-blood without any problems.

36. DIFFERENCES BETWEEN
ABO and Rh
ABO GROUP
•Natural antibodies
•Antibodies are of IgMtype
•Antibodies cannot cross
the placenta
•Antigen is presentin other
tissues
•Secretors are present
•ColdAntibodies(5-20
o
C)
•No recessive gene
Rh GROUP
•Antibodies produced only by
sensitization
•Antibodies are of IgGtype
•Antibodies can crossthe
placenta
•Antigen not presentin other
tissues
•No secretors
•WarmAntibodies (35
o
C)
•Recessive genes are
present

37. IMPORTANCE OF Rh factor
•The discovery of Rh factor made it
possible to understand and to prevent
certain accident caused by blood
transfusion
•Understanding and preventing
hemolytic disease of the newborn –
Erythroblastosis foetalis

38. ERYTHROBLASTOSIS FETALIS
•DISEASE OF FOETUS OR NEWBORN
•Due to development of Rh incompatibility
between the mother and the foetus
•Important only when Rh negative mother
carries Rh positive foetus

39. ERYTHROBLASTOSIS FETALIS
•If mother is Rh –ve and father is Rh + ve
the foetus has a chance to be Rh + ve
•Feto-maternal leak(can occur late weeks of
pregnancy or during delivery) sensitizes the
mother’s immune system to produce Rh
antibodies
•As they are of IgG typethey cross the
placentaand react with the red cells of the
foetus and can cause hemolysis

40. ERYTHROBLASTOSIS FETALIS
•It will take 6 –8 weeksfor antibodies to develop
•By that time the baby is born and usually the first
baby is not affected
•When the mother conceives a Rh +ve baby for
the second time the antibodies cause hemolysis
of RBCs in the fetus
•Produces anaemia, jaundice and edema
(hydrops fetalis)

42. ERYTHROBLASTOSIS FETALIS
•Anaemia stimulate erythropoiesis
•Erythroblasts are formed
•Hence called ERYTHROBLASTOSIS FETALIS
•Enlargement of liver and spleen
•Jaundicedue to hemolysis and accumulation of
bile pigments(cross the blood brain barrier and
get deposited in the basal ganliaproduce
kernicterusand can produce motor disturbances)

43. History of blood group
•Starts with HIPPOCRATES in 17
th
century
•‘PHLEBOTOMY’ is the treatment for diseases
•Discovery of circulation by ‘WILLIAM HARVEY’
in 1628
•First transfusion was carried out in 1665 by
british Phycisian ‘RICHARD LOWER’
•Both donar and recipient were dogs
•SUCCESSFUL

44. History of blood group
•First transfusion on human on a
volunteer in 1667
•Donor was sheep –successful
•“JEAN BAPTISTE DENIS” carried out sheep
to man transfusion –successful
•Third was failure –patient died

45. History of blood group
•First human to human transfusion before the
discovery of blood groups
•By BRITISH PHYSIOLOGIST and
OBSTETRITIAN ‘JAMES BLUNDELL in 1817
•For PPH
•1873 ‘L.LANDOIS’ Physiologist –analyzed the
transfusion done till then and concluded that
HUMAN SHOULD RECEIVE ONLY MUMAN
BLOOD

46. History of blood group
•Blood transfusion is the only remedy
for blood loss
•Blood from certain person produced
reaction when transfused to another
person

47. History of blood group
•He found that mixing of
blood from two individuals
can lead to blood clumping
due to some substance
present in blood
•The clumped RBCs can
crack and cause toxic
reactions
•This can be fatal

48. History of blood group
•Landsteiner identified that
presence of some substance
on the red cell membrane is
the cause for the reaction
•It is the ABO system –Antigen
Antibody reaction

49. Source of antigens
•Antigens are proteins very similar to A and
B are common in intestinal bacteria and in
food for which the newborns are exposed
•Infants rapidly develop antibodies against
the antigens not present in their own cells
•A type individuals develop Anti B antibodies
•B type individuals develop Anti A antibodies

50. GENETIC DETERMINATION OF
BLOOD GROUP
BLOOD GROUPGENOTYPE
GENE FROM
PARENT
OOO*O + O
ABAB”A + B
BBB* or BO”B+B or B+O
AAA* or AO”A+A or A+O
* homozygous transmission ” heterozygous transmission

51. Inheritance of ABO and
Rh(D)
Mother
Group A AO
Rh(D) pos Dd
Father
Group B BO
Rh(D) pos Dd
Group A AO
Rh(D) pos Dd /DD
Group B BO
Rh(D) pos Dd /DD
Group O OO
Rh(D) neg dd
Group A AO
Rh(D) neg dd
Group O OO
Rh(D) pos Dd /DD
Group B BO
Rh(D) neg dd

52. Dominant gene?
•This means ifa person inherited one A
group gene and one B group genetheir
red cells would possess both the A and B
blood group antigens.
•The alleles were termed A ( which produced
the A antigen )
•B (which produced the B antigen)
•O (which was "non functional"and produced
no A or B antigen)

53. SECRETORS & NON SECRETORS
•A and B antigens are not limited to the
red cells
•They are present on the other cellsalso
•They are water soluble
•Secreted in the body fluids
•The persons are called secretors(80%)
•In non secretors they are confined to
the red cells

54. LOCATION OF THE GENE
•The ABO blood group phenotype is
determined by alleles on two
chromosomes
•Chromosome 9–ABO gene allele
•Chromosome 19–Gene that codes for
the creation of the substrate antigen

55. AUTOSOMAL CHROMOSOME
Mustafa
Sara
one alleles from Mustafa and one
from Sara.
The alleles for Blood
group are in the same
place on the
chromosome 9. However
the genes have a
different code giving the
different blood group
A B

56. CODING OF THE GENE
•Both these genes do not code for the actual
antigen
•These genes code for enzymes that create the
antigen on a precursor structure on the red cell
•These enzymes determine a persons ABO
blood group by catalyzing the attachment of a
blood group defining sugar onto a basic
carbohydrate precursor antigen

58. A and B Antigens
•Complex oligosaccharides
•Differs in terminal sugars
•Attached to the RBC membrane ceramide
•H is the basic antigenic structure
•H gene codes for a fucose transferase
that puts a fucose on the end of
glycoprotein forming the ‘H’ antigen
•‘H’ Antigen is present in all blood type

59. Fucose
Transferase
Chr 19
RBC

60. STRUCTURE OF “O”ANTIGEN
•The O blood group
results from the gene at
the ABO locus on
chromosome 9 producing
an enzyme with no
transferase activity
•As a result blood group O
people are not able to
modify the H antigen
RBC

61. STRUCTURE OF “A”ANTIGEN
•The A antigen is produced
by the action of an enzyme
Glycosyl transferasecoded
on chromosome 9 at the
ABO gene locus
•Addition of the sugar
N Acetyl Galactosamineto
the terminal galactose
•Can only produce the A
antigen if a H antigen is
already present
Glycosyl transferase
RBC

62. STRUCTURE OF “B”ANTIGEN
•The B antigen is produced
by an enzyme Glycosyl
transferasecoded by a
gene at the ABO locus on
chromosome 9
•The enzyme catalyses the
addition of the sugar
galactoseto the terminal
galactose of the H antigen.
•The B enzyme can only
producethe B antigen if a
H antigen is present
Glycosyl transferase
RBC

63. •The H antigen is
precursor to the A and
B antigens
•Only recessive alleles
for the H antigen are
inherited (hh)
•The H antigen will
not be produced

64. INHERITANCE OF ‘ABO’ GROUPS
•The agglutinogen A and B are inherited
as Mendelian dominant
•First appear in the sixth week of fetal life
•The concentration at birth is 1/5
th
the
adult level and it progressively rises
during puberty and adolescence
•The agglutinins at birth almost zero
•Appear on 10
th
day of lifeand rises to
peak at 10 years