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BLOOD GROUPS

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INTRODUCTION

Blood is categorized into different groups based on their antigenic properties. Anti-genic& immunologic properties of blood have clinical, genetic & medicolegal importance.

Karl Landsteiner discovered blood groups.


There are around 23 blood group systems containing more than 400 antigens. Of these 400 antigens, only about 30 occur commonly & most of them are weak antigens.

The chief blood groups are:

Classical ‘ABO’ blood groups

Rhesus (Rh) blood group

M & N blood group


CLASSICAL ‘ABO’ BLOOD GROUPS

• The individuals are divided into 4 major blood groups depending on the presence or absence in their RBCs membrane of the blood group specific substance called A, B & O.

• The groups are correspondingly called as given in table & fig.


• A & B are group specific substances, polysaccharide in nature. They are called antigen (agglutinogen) i.e. in the presence of a suitable antibody (agglutinin or ‘isohaemagglutin’) cause clumping of RBCs (agglutination).

• The agglutinin acting on agglutinogen A is called ‘α’ or ‘Anti-A’, the agglutinin acting on agglutinogen Bis called ‘β’ or ‘Anti-B’.


• Group specific substance ‘O’ does not normally act as an agglutinogen & there is no corresponding agglutinin; that is why group ‘O’ RBCs are not agglutinated by agglutinins α or β. The agglutinin α & β are globulins of IgM type & cannot cross the placenta.


• Based on these facts Karl Landsteiner in 1900 framed a law, called Landsteiner’s law. It has two major components:

1) If an agglutinogen is present in the RBCs, of an individual, the corresponding agglutinin must be absent from thr plasma;

2) If the agglutinogen is absent in the individual RBCs, the corresponding agglutinin must be present in the plasma.


• Exception to the 2nd part are: absence of Rh , M& N agglutinogens from the RBCs Which are not accompained by presence in the plasma of anti-Rh, anti-M or anti-N agglutinins.

• Taking into account both agglutinogen & agglutinin, therefore, the full description of four blood groups is Aᵦ; Bα; AB & Oαᵦ. The agglutinin α is subdivided into:

α₁ - agglutinate only A₁

α proper – agglutinate both A₁ & A₂.www.ladderofsuccesstips.com

DETERMINATION OF CLASSICAL BLOOD GROUPS

These can be determined by mixing a drop of isotonic saline suspension of subject’s RBCs with a drop of serum A & serum B separately on a glass slide; & seeing whether agglutination occurs or not. The results are diagnostic.



IMPORTANT NOTE

With high agglutinin titre the cells are massed into a few large clumps; with weaker agglutinin titre more numerous but smaller

clumps are formed.

INHERITANCE OF CLASSICAL ‘ABO’ BLOOD GROUPS

• The Agglutinogen A & B are inherited as Mendelian dominant & first appear in the 6th

week of foetal life. Their concentration at birth is 1/5th the adult level & it progressively rises during puberty & adolescence

• Group specific substances A& B are not limited to the RBCs but are also found in many organs like salivary glands & pancreas (++); kidney, urine, liver & lungs. (+), testes, semen & amniotic fluid.

• The antigens very similar to A & B are common in intestinal bacteria & food to which infants are exposed; & infants rapidly develop antibodies against those antigens which are not present in their own RBCs i.e. either α or βor αβ or none.

• The specific agglutinins are present in the plasma & appear at 10th day, rise to peak at 10 years;& then decline.


• The specific agglutinins act best at low temperature (between 5°C to 20°C , called Cold antibodies. & against well –diluted cells; with weak serum & high cell concentrations the cell may “mop up” agglutinin with out being agglutinated.

• The 4 classical ABO blood groups depend on 3 genes, named after the corresponding factor A,B & O. Each person’s blood group is determined by the two genes which he receives from each parent.



IMPORTANT NOTE

Genes A & B may be demonstrated by the use of anti A or anti B serum. The presence of

‘O’ gene is not easily demonstrated; & to anti-A serum

AA & AO cells react alike, both serologically being group A.

RHESUS (Rh) BLOOD GROUP

• Discovered by Landsteiner & weiner in 1940.

• RBCs of Rhesus monkeys (monkeys with red ischial callosity) when injected into rabbits, the rabbits respond to the presence of antigen in these cells by forming an antibody which agglutinates Rhesus RBCs.


• If the immunized rabbit’s serum is tested against human RBCs, agglutination occurs in 85% of people, these are called Rh ‘+’ (positive) & their serum contains no Rhantibody .

• No agglutination occurs in 15% , these are called Rh ‘-’ (negative) & their serum also contain no Rh antibody.

• The Rh blood group system has not been detected in tissues other than RBCs.


• There are six agglutinogens in Rh system. They are C,D,E,c,d,e. Out of the six agglutinogens only D agglutinogen is potent & therefore Rh group is described only in relation to D agglutinogen.

• Individual having D agglutinogen are said to be Rh+ (positive) & individuals not having D agglutinogen are said to be Rh- (negative) .

• About 85% of the population is Rh+ & 15% of the polpulation is Rh-.


APPLIED PHYSIOLOGY

Rh Incompatibility:

• An Rh- individual transfused with Rh+ blood develops anti Rh agglutinins slowly.

• If this person is later exposed to Rh+ blood, severe transfusion reactions occur.


ERYTHROBLASTOSIS FOETALIS

• This ia a disease of neonates with Rhincompatability. There is agglutination & destruction of foetal red cells.

• In this condition, mother is Rh- & foetus is Rh+ there is no complications in first pregnancy but problem occurs in subsequent pregnancies.


• If Rh+ baby is born to an Rh- mother, some foetal erythrocytes pass to the mother during child birth.

• This produces anti-D antibodies in the mother. In the next pregnancy, if the foetus is Rh+, these antibodies from the mother destroy foetal erythrocytes leading to hemolytic disease of the newborn.


CLINICAL FEATURES

• The foetus is jaundiced, anaemic, liver & spleen are enlarged.

• Increased concentration of bilirubin in the brain tissue can damage the nerve cells leading to kernicterus.

• In severe form it presents as hydrops foetalis.


PREVENTION:

• Administration of anti-D antibodies to the mother soon after delivery of the first child.

• This cause destruction of Rh+ foetal cells in maternal blood.

TREATMENT: Replacement of blood of the new born with Rh- blood repeatedly during the first few weeks.

• About 400mL of Rh- blood is infused & at the same time equal amount of Rh+ neonatal blood is removed.


HEMOLYTIC DISEASES OF NEWBORN

Hydrops Foetalis: The foetus is grossly oedematous, it either dies in utero or if born prematurely or at term, it dies within a few hours.

Icterus Gravis Neonatorum: Characteristic features: The infant born at term is jaundiced or becomes so in 24 hours, due to excessive destruction of RBCs (hemolytic jaundice).


• There may be no anaemia at birth, but develops in a few days. Because at birth, excessive destruction of RBCs is compensated for by an intense normoblastic respone of the marrow, associated with high reticulocytecount & presence of many nucleated RBCs in the circulation (erythroblastaemia or erythroblastosis foetalis).

• There may be severe neurological lesions involving basal ganglia. As blood brain barrier is not developed in foetus & newborn infants, bile pigments enter the brain & they secondarily become stained bright yellow with bile pigment (kernicterus)

• It usually develops when serum bilirubin level exceeds 18mg/dL.

• Liver may also be severely damaged & death may occur from liver failure.

TREATMENT: Exchange blood transfusion soon after birth i.e. removing small quantities of infant’s blood successively from IVC (by passing a polythene catheter along the umbilical vein) & replacing an equal volume of compatible Rh- blood. Thus, infant Rh + RBCs prone to destruction are removed from the circulation.


PREVENTION OF Rh HEMOLYTIC DISEASE:

• Destruction of Rh+ foetal cells in the maternal blood can be broughtabout by admininsteringa single dose of anti-Rh antibodies in the form of Rh-immunoglobulin before or soon after child birth. This prevents active antibodies formation by the mother.

• These antibodies bind to & inactivate the foetal Rh-antigens before mother immune system can produce her own anti-Rhantibodies.


M & N BLOOD GROUPS

• M & N factors depend on two minor genes. Each person carries two of the gene of the M & N group i.e. M+M (=M); N+N (=N) OR M+N (=MN).

• These are antigenic to rabbits.


USES OF BLOOD GROUPING TESTS

• In blood transfusion

• In pregnancy (Rh incompatibility)

• Investigating cases of paternity dispute

• Medicolegal value

• Blood group antigens help in cell recognition


BLOOD TRANSFUSION

• It is a procedure in which blood collected from the donor is transfused to the recipient.

INDICATIONS:

• Sudden blood loss due to accidents

• Duringmajor surgeries

• Patients with bleeding disorders

• Patients with severe burns

• Patients with severe anaemia, thalassemia & leukemia

• Hemolytic disease of new born.

Collection & Storage of Blood:

• Blood is collected from a healthy donor free of all infectious diseases like HIV, hepatitis, malaria & syphilis.

• It is collected under strict aseptic precautions & mixed with anticoagulant (acid citrate dextrose).

• One unit of blood (40mL) can be collected from a donor at a time. This is stored at 2-4°C in blood bank. The stored blood has to be used within 3 weeks from the time of its collection.


• Leukocytes & platelets are absent after 24h of storing blood. Therefore patients requiring leukocytes or platelets should be transfused fresh blood.

Precautions During Blood Transfusion:

• Temperature of the blood to be transfused must be brought to room temperature

• Transfusion should be done under strict aseptic precautions

• Transfusion must be very slow since rapid infusion can lead to excessive load on the heart resulting in cardiac failure.

BLOOD GROUPING & CROSS MATCHING

• Blood grouping & cross matching has to be done to prevent complications blood transfusion.

Blood Grouping: Saline suspension of RBC is mixed with anti-A, anti-B, & anti-D sera.

Presence or absence of agglutination helps to identify the blood group.


• Cross-Matching: Erythrocyte of the donor is matched with serum of recipient in major cross-matching.

• In minor cross-matching erythrocyte of recipient is matched with serum of the donor.


Hazards of Blood Transfusion: Hazards of Mismatched Blood Transfusion

• Immediate Effect: This includes hemolysisleading to shock & renal failure due to precipitation of Hb in the nephrons.

• Hemolysis: Mismatched blood transfusion results in antigen- antibody reaction inside the recipient’s body causing massive destruction of red blood cells.


• Shock: This is caused due to loss of circulating RBCs & also production of toxic substances from the hemolyzed cells. The arterial pressure falls leading to decreased renal blood flow.

• Renal failure: This occurs within few minutes to few hours of blood transfusion.

• Renal failure is due to constriction of renal blood vessels by toxins released,

• Reduced blood flow secondary to circulatory shock, &

• Precipitation of Hb in the nephrons.

• Delayed Effect Jaundice: occurs due to release of haemoglobin from hemolyzed RBCs

• Haemoglobin released is converted to bilirubin .

• Bilirubin concentration in the body fluids increases resulting in jaundice.


Other Hazards Of Blood Transfusion

• Immediate: Pyrogen reactions, shock, circulatory overload, hyperkalemia, hypocalcemia.

• Delayed: Transmission of diseases, & iron overload.

• Pyrogen Reactions: Fever with chills & rigors can develop during transfusion.


• Circulatory Overload: Rapid transfusion of blood can lead up hypervolemia resulting in circulatory overload.

• Hyperkalemia: This occurs due to loss of K⁺ ions from red cells into plasma in stored blood

• Hupocalcemia: Addition of citrate to blood results in lack of ionized calcium resulting in hypocalcemia.


• Transmission of Diseases: Malaria, Syphilis, & HIV can be transmitted through blood.

• Iron Overload: This occurs in patients receiving repeated blood transfusion.

Autologous Blood Transfusion: This refers to transfusion of an individual’s own blood which has been drawn earlier & stored. Around 1-1.5L of blood can be withdrawn over a period of 3 weeks. This can be used in case of elective surgeries.



DR.LUCKY

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