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What is a blood group?

• Any variation or polymorphism "having
  multiple forms". detected in the blood could
  be considered a blood group, restricted to
  blood cell surface antigen generally to red cell
  surface antigen
Nomenclature
• The ABO blood group system was discovered by          Karl Land
  Steiner in 1901.

    Red blood cells or erythrocytes are present in the blood and
    contain certain proteins on their surface.
•   These proteins are called antigens.
•   The plasma which is the liquid part contains antibodies which
    will attack certain antigens if they are present.
•   There are various types of red blood cell antigens - the ABO
    and rhesus types are the most important.
•   By the time a person is six months old, he naturally will have
    developed antibodies against the antigens his red blood cells
    lack.
Blood Group “A”
• A blood group
  individuals will have
  type A antigens on the
  surface of red blood
  cells
• And anti-B antibodies in
  plasma
Blood Group “B”
• B blood group
  individuals will have
  type B antigens on the
  surface of red blood
  cells
• And anti-A antibodies in
   plasma.
Blood group AB

• AB blood group are those
  who will have type A and
  type B antigens on the
  surface of red blood cells
• And no antibodies to A or B
  antigens in plasma.
Blood group “O”
• O blood group are
  those who will have
  neither type A or type B
  antigens on the surface
  of red blood cells
• but will have anti-A and
  anti-B antibodies in
  plasma.
1.   The reason for the presence
     of A and B antibodies in blood
     is not clearly understood.
2.   Antibody normally do not
     developed against unless the
     body is exposed to the
     antigen.
3.   This means, for example, that
     a person with type A blood
     should not have type B
     antibodies unless he has
     received a transfusion of type
     B blood, which contain type B
     anti-gens
• Because people with type A blood (who never have
  received a transfusion of type B blood) do have type
  B antibodies,
• One possibility is that type A or type B antigens on
  bacteria or food in the digestive tract stimulate the
  formation of antibodies against antigens that are
  different from one's own antigens.
• Thus a person with type A blood would produce type
  B antibodies against the B antigens on the bacteria
  or food.
• In support of this hypothesis is the observation that
  A and B antibodies are not found in the blood until 2
  months after birth
• Agglutinins
• Agglutinins
Donor and recipient
• A donor is a person who give blood
• A recipient is a person who received blood
•
• The six possible           O   47%
  combinations of genes,
  as shown in are OO, OA,
                             A   41%
  OB, AA, BB, and AB.
  These combinations of
  genes are known as the     B   9%
  genotypes, and each
  person is one of the six
  genotypes.                 A   B3%
•
    A general view of the molecular
    structure of Elizabethkingia
    meningosepticum N-
    acetylgalactosaminidase in
    complex with the NAD+ cofactor
    (in yellow) and the A antigen on
    the surface of A type red blood
    cells. The N-acetylgalactosamine
    molecule recognized and
    hydrolyzed by the enzyme
    appears in red. (Credit: Copyright
    AFMB - CNRS 2007)
Rhesus factor
           History of discoveries

• The Rhesus system is named after the Rhesus
  monkey, following experiments by Karl Land steiner
  and Alexander S. Wiener, which showed that rabbits,
  when immunised with rhesus monkey red cells,
  produce an antibody that also agglutinates the red
  blood cells of many humans. This factor was
  discovered in 1937 (publishing in 1940)
Rhesus factor

• Individuals either have, or do not have, the Rhesus factor (or
  Rh D antigen) on the surface of their red blood cells.
• This is usually indicated by 'RhD positive' (does have the RhD
  antigen)
• or 'RhD negative' (does not have the antigen)
• This suffix is often shortened to 'D pos'/'D neg', 'RhD pos'/RhD
  neg', or +/-.
• RhD+
• or RhD-
• In simplest terms, there may be prenatal danger to the fetus
  when a pregnant woman is RhD-negative and the biological
  father is RhD-positive.
• Rh + father      Rh- mother




                Rh+fetus
Hemolytic disease of the newborn

• Hemolytic disease of the newborn is also called
  Erythroblastosis Fetalis. This condition occurs when
  there is an incompatibility between the blood types
  of the mother and the baby..
• hemolytic comes from two words: hemo (blood) and
  lysis (destruction) or breaking down of red blood
  cells
• erythroblastosis refers to the making of immature
  red blood cells
• fetalis refers to the fetus
   When the condition is caused
    by the RhD antigen-antibody
    incompatibility, it is called
    RhD Hemolytic disease of
    the newborn (often called
    Rhesus disease or Rh
    disease
   Here, sensitization to Rh D
    antigens (usually by feto-
    maternal transfusion during
    pregnancy) may lead to the
    production of maternal anti-
    RhD antibodies which can
    pass through the placenta.
    This is of particular
    importance to RhD negative
    females because any
    subsequent pregnancy may
    be affected by the Rhesus D
    hemolytic disease of the
    newborn if the baby is Rh D
    positive.
•   Fetal-maternal hemorrhage can
    occur due to trauma, abortion,
    childbirth, ruptures in the
    placenta during pregnancy, or
    medical procedures carried out
    during pregnancy that breach
    the uterine wall.
•   In subsequent pregnancies, if
    there is a similar incompatibility
    in the fetus, these antibodies
    are then able to cross the
    placenta into the fetal
    bloodstream to attach to the
    red blood cells and cause
    hemolysis.
•    In other words, if a mother has
    anti-RhD antibodies as a result
    of previously carrying a RhD-
    positive fetus, this antibody will
    only affect a fetus with RhD-
    positive blood.
• The vast majority of Rh disease is preventable in
  modern antenatal care by injections of IgG anti-D
  antibodies (Rh(D) Immune Globulin).
• The incidence of Rhesus disease is mathematically
  related to the frequency of RhD negative individuals
  in a population, so Rhesus disease is rare in East
  Asians and Africans,
• but more common in Caucasians.
Population data
The frequency of Rh factor blood types and the RhD neg allele gene differs in
various populations.

]



Population data for the Rh D factor and the RhD neg allele

Population           Rh(D) Neg                     Rh(D) Pos

European Basque      approx 35%                    65%

Caucasian            Approx 35 %                   65%

American Blacks      approx 35%16%approx           65%84%93%99%over
                     7%approx 1%less 1%less 1%     99%over 99%
Native American      approx 35%16%approx           65%84%93%99%over
Indians              7%approx 1%less 1%less 1%     99%over 99%

African descent      approx 35%16%approx           65%84%93%99%over
                     7%approx 1%less 1%less 1%     99%over 99%
Symptoms and signs in the Fetus:

    Enlarged liver, spleen, or heart and fluid buildup in the fetus' abdomen
         seen via ultrasound.
•    Symptoms and signs in the Newborn:
    1.   Anemia which creates the newborn's pallor (pale appearance).
    2.   Jaundice or yellow discoloration of the newborn's skin, sclera or
         mucous membrane. This may be evident right after birth or after 24
         - 48 hours after birth. This is caused by bilirubin (one of the end
         products of red blood cell destruction).
    3.   Enlargement of the newborn's liver and spleen.
    4.   The newborn may have severe edema of the entire body.
    5.   Dyspnea or difficulty breathing.
Blood group

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Blood group

  • 1.
  • 2. 2
  • 4. What is a blood group? • Any variation or polymorphism "having multiple forms". detected in the blood could be considered a blood group, restricted to blood cell surface antigen generally to red cell surface antigen
  • 5. Nomenclature • The ABO blood group system was discovered by Karl Land Steiner in 1901. Red blood cells or erythrocytes are present in the blood and contain certain proteins on their surface. • These proteins are called antigens. • The plasma which is the liquid part contains antibodies which will attack certain antigens if they are present. • There are various types of red blood cell antigens - the ABO and rhesus types are the most important. • By the time a person is six months old, he naturally will have developed antibodies against the antigens his red blood cells lack.
  • 6.
  • 7. Blood Group “A” • A blood group individuals will have type A antigens on the surface of red blood cells • And anti-B antibodies in plasma
  • 8. Blood Group “B” • B blood group individuals will have type B antigens on the surface of red blood cells • And anti-A antibodies in plasma.
  • 9. Blood group AB • AB blood group are those who will have type A and type B antigens on the surface of red blood cells • And no antibodies to A or B antigens in plasma.
  • 10. Blood group “O” • O blood group are those who will have neither type A or type B antigens on the surface of red blood cells • but will have anti-A and anti-B antibodies in plasma.
  • 11. 1. The reason for the presence of A and B antibodies in blood is not clearly understood. 2. Antibody normally do not developed against unless the body is exposed to the antigen. 3. This means, for example, that a person with type A blood should not have type B antibodies unless he has received a transfusion of type B blood, which contain type B anti-gens
  • 12. • Because people with type A blood (who never have received a transfusion of type B blood) do have type B antibodies, • One possibility is that type A or type B antigens on bacteria or food in the digestive tract stimulate the formation of antibodies against antigens that are different from one's own antigens. • Thus a person with type A blood would produce type B antibodies against the B antigens on the bacteria or food. • In support of this hypothesis is the observation that A and B antibodies are not found in the blood until 2 months after birth
  • 13.
  • 15.
  • 16. Donor and recipient • A donor is a person who give blood • A recipient is a person who received blood •
  • 17.
  • 18. • The six possible O 47% combinations of genes, as shown in are OO, OA, A 41% OB, AA, BB, and AB. These combinations of genes are known as the B 9% genotypes, and each person is one of the six genotypes. A B3%
  • 19.
  • 20.
  • 21.
  • 22. A general view of the molecular structure of Elizabethkingia meningosepticum N- acetylgalactosaminidase in complex with the NAD+ cofactor (in yellow) and the A antigen on the surface of A type red blood cells. The N-acetylgalactosamine molecule recognized and hydrolyzed by the enzyme appears in red. (Credit: Copyright AFMB - CNRS 2007)
  • 23. Rhesus factor History of discoveries • The Rhesus system is named after the Rhesus monkey, following experiments by Karl Land steiner and Alexander S. Wiener, which showed that rabbits, when immunised with rhesus monkey red cells, produce an antibody that also agglutinates the red blood cells of many humans. This factor was discovered in 1937 (publishing in 1940)
  • 24. Rhesus factor • Individuals either have, or do not have, the Rhesus factor (or Rh D antigen) on the surface of their red blood cells. • This is usually indicated by 'RhD positive' (does have the RhD antigen) • or 'RhD negative' (does not have the antigen) • This suffix is often shortened to 'D pos'/'D neg', 'RhD pos'/RhD neg', or +/-. • RhD+ • or RhD- • In simplest terms, there may be prenatal danger to the fetus when a pregnant woman is RhD-negative and the biological father is RhD-positive.
  • 25. • Rh + father Rh- mother Rh+fetus
  • 26. Hemolytic disease of the newborn • Hemolytic disease of the newborn is also called Erythroblastosis Fetalis. This condition occurs when there is an incompatibility between the blood types of the mother and the baby.. • hemolytic comes from two words: hemo (blood) and lysis (destruction) or breaking down of red blood cells • erythroblastosis refers to the making of immature red blood cells • fetalis refers to the fetus
  • 27. When the condition is caused by the RhD antigen-antibody incompatibility, it is called RhD Hemolytic disease of the newborn (often called Rhesus disease or Rh disease  Here, sensitization to Rh D antigens (usually by feto- maternal transfusion during pregnancy) may lead to the production of maternal anti- RhD antibodies which can pass through the placenta.  This is of particular importance to RhD negative females because any subsequent pregnancy may be affected by the Rhesus D hemolytic disease of the newborn if the baby is Rh D positive.
  • 28. Fetal-maternal hemorrhage can occur due to trauma, abortion, childbirth, ruptures in the placenta during pregnancy, or medical procedures carried out during pregnancy that breach the uterine wall. • In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause hemolysis. • In other words, if a mother has anti-RhD antibodies as a result of previously carrying a RhD- positive fetus, this antibody will only affect a fetus with RhD- positive blood.
  • 29.
  • 30. • The vast majority of Rh disease is preventable in modern antenatal care by injections of IgG anti-D antibodies (Rh(D) Immune Globulin). • The incidence of Rhesus disease is mathematically related to the frequency of RhD negative individuals in a population, so Rhesus disease is rare in East Asians and Africans, • but more common in Caucasians.
  • 31. Population data The frequency of Rh factor blood types and the RhD neg allele gene differs in various populations. ] Population data for the Rh D factor and the RhD neg allele Population Rh(D) Neg Rh(D) Pos European Basque approx 35% 65% Caucasian Approx 35 % 65% American Blacks approx 35%16%approx 65%84%93%99%over 7%approx 1%less 1%less 1% 99%over 99% Native American approx 35%16%approx 65%84%93%99%over Indians 7%approx 1%less 1%less 1% 99%over 99% African descent approx 35%16%approx 65%84%93%99%over 7%approx 1%less 1%less 1% 99%over 99%
  • 32. Symptoms and signs in the Fetus: Enlarged liver, spleen, or heart and fluid buildup in the fetus' abdomen seen via ultrasound. • Symptoms and signs in the Newborn: 1. Anemia which creates the newborn's pallor (pale appearance). 2. Jaundice or yellow discoloration of the newborn's skin, sclera or mucous membrane. This may be evident right after birth or after 24 - 48 hours after birth. This is caused by bilirubin (one of the end products of red blood cell destruction). 3. Enlargement of the newborn's liver and spleen. 4. The newborn may have severe edema of the entire body. 5. Dyspnea or difficulty breathing.