BLOOD GROUPS

On the surface of plasma membrane of RBCs,

certain glycoproteinous molecules, called antigens,
are present. These antigens differ in different persons
and give specific blood grouping to them. Two very
are
important and common types of blood groups
1. ABO blood groups.
2. Rh-Blood group systen.
1. ABO-Blood groups
A German biochemist, Karl Landsteiner (1901),
on the basis of the blood-transfusion results, proposed
that blood of different persons has some biochemical
differences. He confirmed the presence of two types of
proteins in the human blood
(a) Agglutinogen or antigens. It is a glycoprotein
present on the surtace of RBCs, also called corpuscle
factor. There are two types of antigens - A and B. A

person may have neither of them or one of them or both.

(b) Agglutinin or antibody. It is ay-globulin protein
present in the blood plasma, so is also called plasmna
factor. There are two types of antibodies-a and b. A
person may have neither of them or one of them or both.
Both antigen 'A and antibody 'a' (also called
Anti-A) are incompatible, and antigen'B' and antibody
b (also called Anti-B) are incompatible to each other.
So these show agglutination when incompatible bloods
come together. On the basis of antigens present, four
types of blood groups have been recognized (Table
The person with O-blood group is called univers
4
donor as it has no antigen and can donate its blood t
to
any person, while the person with AB-blood
group is
called universl recipient as it has no antibody in their
plasma so can receive blood from any blood group
Table 4 shows that
(a) Blood group A has A-antigen and b-antibody.
(b) Blood group B has B-antigen and a-antibodv
(c) Blood group AB has both A and B antigens but
no antibody.
(d) Blood group O has no antigen but with both
antibodies.
Knowledge of bl0od groups is used in safe blood
transfusion so that the corpuscle factor of the donors
blood must be compatible with the plasma factor
of recipient. If incompatible, then donor's blood is
agglutinated. Safest blood for blood transfusion is
ABO-Incompatibility during blood transtuston
Blood transfusion involves the transfer of blood frot
one person to another. When an incompatible bloOu
transfused (e.g., Donor with B-blood group and reciple
ient
with A-blood group vice versa), then reaction Occ
or
between donor's antigen and recipient's
antibody causi
the clumping of donor's blood inside the blood vesseels
of the recipient resulting in
blockage of the blood ves
which may be fatal to the recipient.
 Table 4. Different types of blood groups.
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Blood Group Antigen Antibody Can give blood to Can receive blood from
Genotype
A b A, AB A, O AA or AO
B a B, AB
B, O BB or BO
AB A, B (Both) None AB All (Universal recipient) AB
O None a, b (Both) All (Universal donor) O OO
 ABO-Incompatibility during pregnancy
Blood group incompatibility between the maternal
blood and foetal blood may cause problems e.g., If
female with A-blood group carries a foetus with B-blood
group. Then antibodies of maternal blood enter the
foetal blood circulation and may destroy red blood cells
of the foetus. This may cause anaemia, jaundice, etc. in
the baby, called haemolytic disease of new born.
2. Rh-Blood group system
Rh-factor is an antigernic protein present on the
surface of red blood cells. It was first discovered by
Landsteiner and Weiner (1940) on the plasma-membrane
of RBCs of rhesus monkey (Macaca rhesus), so is called
Rh-factor (also called D-antigen). Later, it was also
found in about 80% of human beings and were called
Rh-positive (Rh). The person with no Rh-factor is
called Rh negative (Rh).
Rh-factor character is controlled by a pair of genes-
R and r. R-gene is dominant and controls the synthesis
 cannot synthesize Rh-factor
Rh-factor
of Rh-factor while r-gene
are:
so different possible genotypes

Phenotype Genotype
RR or Rr
Rh-positive
rr
Rh-negative
Incompatibility of Rh factor during pregnancy
Rh-incompatibility is a condition that develops
when a pregnant woman has Rh-negative blood and the
baby in her womb has Rh-positive blood. The child of a
homozygous Rh-positive male and his Rh-negative wie
will always be Rh-positive. Rh+ child develops in the
womb ofa Rh-mother. When foetal and maternal bloou
come closer during placenta cutting after child birth,
then some foetal RBCs with Rh-antigen of the developin
foetus enter the maternal blood and stimulates her
WBCs h
to produce antibodv called anti-Rh-factor
remains effective in maternal
blood for severai month
OyearS. First born infants are usually not affecte and
and

are
born normal because it takes time for nother
 to
develop antibodies. But from the second pregnancv
onward, the accumulated antibodies from the maternal
blood enter the foetal blood and cause
agglutination of
foetal blood cells. This is called erythroblastosis foetalis
(Fig. 5) and causes the immediate death of the baby due
to congestive heart failure,
hepatosplenomegalv, severe
haemolvticanemia and jaundice, or a tew davs atter the
birth due to overproduction ofbilirubin which
damages
the babys brain. In such cases, blood-transtusion of
baby just after the birth is recommended. No
during
the second trimester ot pregnancv, the mother is
given
an intramuscular injection of anti-Rh
antibodies, called
Rh-immunoglobulin (Rhg) or Rhogam. (commonly
called Rho (D) Ig Therapy). If the
the mother is
baby is Rh-positive,
given second injection within a tew davs
after delivery. These antibodies destroy foetal cells that
got into her circulation betore thev can initiate an active
immune response in her.
No abnormalitv arises when the wife
is-Rh-positive
and her husband is Rh-negative.
Coombs Test is used to detect if
antibodies or complement SVstem tactors
have been bound to RBCs surface antigens
111 ITo. Coombs reagent contains antihuman

globulin (antibodies). It is employed to

detect hemolytic disease of new born and
d number of other hamolytic diseases.

Internationa-
 incompatibility of Rh factor in blood transfusion
Human blood does not contain
any antibody for Rh
factor. However, if the blood of a Rht
donor is injected
into the blood of a Rh recipient in blood
transfusion,
anti-Rh antibody is formed and gradually accumulates in
the blood of the recipient. But no Complication occurs in
the recipient after the first transtusion. Any Subsequent
transfusion of Rh*
blood to the same patient will cause
clumping of donor's RBCs in recipient's body, causing
blocking of blood capillaries and death.
 BLOOD CLOTTING/ COAGULATION
1. Definition. The property of blood to change from
fluid to gel state when coming in contact with air is
called blood coagulation or blood clotting.
2. Aim. To prevent excessive loss of blood from an
injury, so is a natural defensive mechanism.
3. Period. The blood clot is
fully formed within 3
to 6 minutes.
4. Mechanism of Blood coagulation. According to
Biggs and Macfarlone (1966), blood clotting is a cascade
mechanism (chain reaction with
multiplication
step) and involves three essential steps:
at everv

A. Formation of Prothrombin
B. Conversion of
Activator.
Prothrombin to thrombin.
C. Conversion of
formation of blood clot. Fibrinogen to fibrin and and
 Faciors involved. According to International Commission on Blood Coagulation (1954), thirteen
CoaguIation factors are involved
. Fibrinogen (Synthesized by liver) II. Prothrombin (Synthesized by liver).
Thrombokinase (Released from injured tissues and blood platelets at injury).
IVCalciumions V.Labile factor
VII. Stable factor or Proconvertin
VI (Not proved so far)
Accelerin
IX. Christmas factor
Vil. Antihaemophilic factor (AHF)
S t u a r t P'rower factor XI. Plasma Thromboplastin Antecedent (PTA)
Surface factor XIII. Fibrin stabilizing factor.
II Hageman or
activated i
precursors, called native form. These
are
these clottin tactors occur as inactive
foto
 Ceogulalue Castad
972
MODERN'S abc+OF BIOLOGY-
(A) Formation of
Prothrombin Activator. It is a G) Extrinsic pathway. This mechanism
combination of activated factors like X, V, begins with
platelet phos- a trauma to the blood vessel and the surrounding tissue
pholipids
is
and calcium. Xa is the fundamental
agent.It and involves three steps (Fig. 6).
formed in two ways:

(a) Injured tissue Snuin Laus)

Blood exposure to collagen of blood vessel
Tissue thrombokinase (a)
XII- Activated XII
(Lipoprotien + phospholipid
(b)
complex ininegen
XI- Activated XI
(c)
(b) VII Vla
(d)
IX Ca
> Activated IX
VIII
X Activated Activated a
(e) Ca
(c) Ca

Prothrombin activator
Platelet phospholipids
and factor I
/
Rap tat ) Prothrombin
anism
Fig. 6.Extrinsic mechanism of
of formation
formation of Fig. 7. Intrinsic mechanism of
formation of
activator
prothrombin activator. prothrombin activ ator
 (ii) Intrinsic pathway. This mechanism begins witha
trauma to blood itself or when the blood comes in
contact
with the collagen of injured blood vessel and
involves a
series of five steps (Fig. 7):
(B) Conversion of Prothrombin into Thrombin
Extrinsic or Intrinsic Prothrombin Activator

Prothrombin t+ Thrombin
Ca

(C) Conversion of Fibrinogen into Fibrin by

thrombin which removes four low mol wt
from fibrinogen to form a fibrin
peptides
monomer.
Thrombin
olule
Fibrin montomer (insoluble)
Fibrinogen
(soluble) Fibrin stabilizing factor (XIII)
Thiernbu
(polymerization)
Fibrin threadsiud)
(mA
Formation of fibrin threads is' very rapid
and takes process
only
10 to 15 seconds.
Fibrin threads
polymerize and form a meshwork which traps, blood
cells, platelets etc. to form a clot or coagulum (Fig. 8)
so the process is called blood clotting. In the
fibrin monomers are joined by weak H-bonds
deginning,
and threads are not cross-linked. This is called soft
clot. But within a few minutes, activated Factor
XIII stimulates the formation of covalent bonds and
cross-linkages by disulphide bonds between fibrin
threads to form dark reddish brown scum called hard
clot. So a blood clot consists of a plug of dead anel
damaged blood cells trapped in a network of insoluble
fibrin molecules.
 ator.
Within a few minutes, the
clot begins to contract and a
pale-coloured fluid called serum A
is formed. This is called
clot-
retraction. Serum differs from AV
blood plasma in being without
blood clotting proteins so cannot
clot the blood. So serum is
basically plasma minus blood
clotting proteins. Fig. 8. Blood clot