BLOOD GROUPS

What is blood groups

 Antigens A BO system
(agglutinogens) on
A antigen B antigen
RBCs membrane
 two major

blood group antigen

systems, namely ABO
Rh system
and Rh.
D antigen
What is blood groups
ABO RH blood
 Blood is grouped or group
classified according to A D A+
types of antigens on A ------ A-
RBC s membrane
B D B+

B ---- B-

AB D AB+

AB ----- AB-

---- D O+

------- ------- O-
ABO system
 Antibodies (agglutinins) against these antigens are
present naturally in the plasma
 Individual’s will form immune antibodies to ABO
blood group antigens they do not possess
 ABO system
Blood group B
Blood group A

Antibodies against Antibodies against

B antigen A antigen
Prevalance in population :41% 10%
 ABO system

Blood group AB Blood group O

No Antibodies Antibodies against

A B antigen
Prevalance in population :4% 45%
 Effect of mixing different blood groups

Blood group B
Blood group A

Antibodies against Antibodies against

B antigen A antigen
Antigen-Antibody reaction (agglutination)
Agglutination
Agglutination and hemolysis
 If an individual is
transfused with an
incompatible blood
group
Surface antigens+ opposing antibodies

 Clumping
agglutination
 Close blood vessels,
ischemia and pain
Agglutination and hemolysis
 Clumped RBCs
phagocytosed and
destructed into RES

agglutination and
hemolysis
Q1:Importance of blood grouping
 Blood transfusion
 Medicolegal : exclude paternity

A, B antigens are coded by dominant genes

Inherited by mandalian rule
A phenotype: AA, AO
B phenotype: BB, BO
AB phenotype: AB OO phenotype: O
Exclude paternity
 Mother  Father
 A  O
 Phenotype: AA AO  Phenotype: OO

 Children
 AO, OO
 Phenotype: O or A
 If child is blood group B this denies paternity
 Blood transfusion
Q2:Indications
1)To restore blood volume after haemorrhge (if more
than 20 % is lost)
2) To replace loss of any of blood components:
Plasma loss as in burn
Plasma protein hypoproteinemia
Red blood cells loss in severe anemia
Erythroblastosis fetalis
White blood cells loss in leucopenia, severe infections
Platelet defect as in purpura
Coagulation factor defect as in haemophilia
 Q3:Precautions taken before blood transfusion

 Insure that Blood is stored in

sterile plastic bag
 Precautions taken before blood transfusion

 The bag is coated with a

mixture of C D P
 C: Citrate prevent coagulation
 D: Dextrose nourish RBCs
 P: Phosphate for ATP
production
 A label is put on the bag
Precautions taken before blood transfusion

 Blood bag label

 1) Donor information
 Name
 Address
 Age
 ID number
 Donation date
Precautions taken before blood transfusion

 Blood bag label

 2)Blood group
Precautions taken before blood transfusion

 Blood bag label

 3) Blood test

 Insure the blood is free

from AIDS, hepatitis C,

malaria

 Check Haemoglobin
level
 Must be not less than
90% of normal
Precautions taken before blood transfusion

 Blood bag label

 4) Expiration date

 Blood is stored at 4co

 Valid for 14-21 days

after donation
 To avoid hazards of

old blood transfusion

Precautions taken before blood transfusion

 Blood bag label

 5) product code (Type,
volume)
Precautions taken before blood transfusion

 Blood bag label

 Additional
information;
BLOOD TYPING
Q4:Blood typing (Slide technique test)

 A dry sterile slide is

needed
 Put a drop of blood on one Anti
side D

 Put a drop of antibodies

on the other side
 Antibodies are previously
prepared against RBC s
antigens inside an Anti Anti
A B
experimental animal)
 Mix both drops together
Q4:Blood typing (Slide technique test)
Blood typing (Slide technique test)

Agglutination No agglutination

 If the RBCs contain the  If an rbc does not have

A antigen the red blood the A antigen there will
cells will be be no clumping, a
agglutinated by anti-A, negative reaction
a positive reaction.
Q5:Cross matching

 Pretransfusion compatibility test

Donor RBCs Recipient RBCs

Donor Serum
Recipient serum
antibodies
antibodies

Agglutination indicates incompatibility

Q6:Dangers of blood transfusion
Immediate:
1-Incompatible blood transfusion
2- Bacterial infection (unhygenic transfusion)
3- Circulatory overload: cardiac patients- massive transfusion
4-Hyperkalemia: leads to ventricular fibrillation especially in old
blood
5-Hypothermia
6-Citrate toxicity: hypocalcemia occur in massive blood transfusion
Delayed:
Blood borne disease transmission
Q7:ABO incompatability
 Donor RBCs
agglutinated by
agglutinins in recipient
plasma
 Donor serum
antibodies will be Donor RBCs
Recipient RBCs
diluted after being
transfused in recipient,
so they rarely cause
Donor Serum
agglutination antibodies
Recipient
serum
antibodies
Q7: Main events following ABO incompatability

 A-clumping of RBCs

 B-Antigen-antibody reaction

 C-Rapid intravascular RBCs haemolysis

 Free Hb Excess K+ Excess histamine

Effect of ABO incompatability
 A-clumping of RBCs
 1-Block blood vessels—severe
pain, dyspnea, chest pain
 B-Antigen-antibody reaction
 2-Fever, chills
 3-Histamine released lead to
generalized hypotension, shock
 Effect of ABO incompatability
 C-Rapid intravascular RBCs haemolysis
Excess histamine
Free Hb +Excess K

Generalized Cardiac arrythmia Filtered through

hypotension, shock kidney tubules, block
renal tubules, renal
failure
Released Hb---
bilirubin--- jaundice

 Stop transfusion, treat renal failure, treat hyperkalemia, give antipyretic


Effect of ABO incompatability
 Renal failure:
 Causes:
 A- Renal tubules blocked by acid hematin
 b –Renal vasoconstriction due to toxic substances
from the hemolysisng RBCs following the antigen-
antibodies reaction of the transfusion reaction.
 c- Circulatory shock from the loss of RBCs and the
production of toxic substances decreasing the
glomerular blood flow and urine output.
Q8: RH incompatibilty
 RH system
 Composed of many antigens(Dd, Cc, Ee, )
 D antigen is the most immunogenic and was
named after the monkeys in which it was first
discovered

 85% RH+ve 15% RH –ve

 RH antibodies
 Produced by exposure to foreign RH Ag
 In complete Ig G
Importance of RH system
 1- blood transfusion:
 An RH –ve person transfused with RH+ve blood
 First transfusion: develop RH AB in his plasma
 Second transfusion: transfused cells agglutinate
by antibodies formed from first transfusion
 2- In pregnancy:
 An RH –ve mother carrying an RH+ve fetus
 Rh incompatability leads to erythroblastosis
fetalis
 Erythroblastosis fetalis
First Mother RH-ve Fetus RH+ve
pregnancy Baby
At delivery time , born
Mother will normal
form RH leak to maternal
antibody circulation

Second Mother RH-ve

pregnancy Fetus RH+ve
Mother plasma contain
RH antibody

RH AB are IG g Fetal RBCs

cross placenta haemolysis
When will the first baby suffer
Mother RH-ve
D antigen introduced to the body
1)Abortion
2)Bleeding during pregnancy
3) Previously transfused with RH+ve

Mother plasma contain First baby (RH +ve)

RH antibody

RH AB are IG g Fetal RBCs

cross placenta haemolysis
Erythroblastosis fetalis
 Clinical picture
 High titre of AB-------IUFD (intra uterine fetal death)
 Severe anemia, odema (hydropis fetalis)
 Haemolysis, jaundice--- bilirubin level increases
(Kernictrus)
 Hepatomegaly, spleenomegaly , acting as another site
of haematopoeisis, to compensate RBCs destruction
 Increased hematopoietic activity--- premature
erythrocytes (erythroblastosis)
Erythroblastosis fetalis
 bilirubin level increase in fetus-----kernictrus
 Normally, BBB (brain blood barrier) prevent
bilirubin from passing to the brain
 But fetal BBB is not well developed, bilirubin will
cross to, deposit in the brain cells
 Mental retardation
Blood vessel lumen
Endothelial

X
Basement
barriermembrane
Astrocytes

 Basal ganglia disorder

Erythroblastosis fetalis

Fetal Brain with yellow

bilirubin deposits

Kernictrus patient with

mental retardation,
motor problems
 prophylaxis
First Mother RH-ve Fetus RH+ve
pregnancy Baby
At delivery time , born
Mother will normal
form RH Destruct leak to maternal
antibody RH circulation
antibody
Within 48 hours Anti- RH antibodies

Second Mother RH-ve

pregnancy Fetus RH+ve
Mother plasma doesnot
contain RH antibody No Fetal
RBCs
haemolysis
Treatment
 phototherapy:
 Alters the bilirubin from a toxic form
to a water soluble, non-toxic form that
can be eliminated.
 Exchange transfusion with o-ve blood:
 400ml Blood slowly infused over 2
hours, while baby's blood is
simultaneously removed
 Remove positive red blood cells,
antibodies, bilirubin