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BLOOD TYPES
Blood cells have
30 commonly antigens and more than 100 rare antigens
Antigens are also called AGGLUTINOGENS
Antibodies are also called AGGLUTININS which are
mostly IgM and IgG
Two major blood group system
1. O-A-B blood group system
2. Rh system
Transfusion reaction
Clumping of red blood
cells as a result of
mismatched blood groups
is called as
AGGLUTINATION
IgG have 2 binding sites
IgM have 10 binding sites
( HEMOLYSINS)
Transfusion reaction
Acute Reactions:
1.Agglutination: due to clumping
2.Hemolysis: due to lytic coplex of complement
3. Allergic reaction: Due to reaction with donors protein
4.Febrile Reaction: Due to pyrogens and wbc
5.Acute kidney shutdown: due to
i. vasoconstrictions because of toxins
ii.loss of recipient RBCs and because of toxins lead to
vasodilation and increased permeability of vessels lead to
circulatory shock
iii. Tubular blockage because of heptoglobin consumption
Delayed reactions
Delayed hemolytic reactions: either physical
rupture of clmped RBC or attack of WBC on
clumbed RBC eads todelayed hemolysis and
release of bilirubin,leads to jundice
Air embolism:
Bacterial contamination
Iron Overload
Ion changes: Hyperkalemia,Hypernatrimia
,Hypocalcemia
Transfusion of disease :e.g Hepatitis
Thrombophlebitis: due to faulty techniue
Products of complement system cause
rupture of donor RBCs & release of free Hb in
the plasma. This is called the Immediate
Response.
Due to agglutination RBCs clog smaller blood
vessels & further phagocytosis by
macrophages causes further release of Hb &
other toxins in the plasma. This is known as
the Delayed Response.
Transfusion reaction
Mismatched blood group always causes agglutination of
Donor red blood cells due to
1. Donor agglutinins are diluted by recipients plasma
2. Recipients agglutinins are not diluted by small amount
of infused blood
Jaundiced is seen when more than 400 milliliters of blood is
hemolyzed in a day
Blood typing
Rh blood type
Six antigens or Rh factors
C, D, E, c, d, e
D antigen presence or absence give positive or negative
blood group
Delayed transfusion reaction
Anti-Rh- Agglutinins develops in 2 to 4 weeks and reaches
its maximum concentration 2 to 4 months later
Erythroblastosis Fetalis
Hemolytic disease of newborn
Characterized by agglutination and
Phagocytosis of fetus’s red blood cells
Father Mother Fetus
Rh +ve Rh-ve Rh+ve from father
Clinical picture
Jaundiced
Anemic
Hepatosplenomegaly
Nucleated Blastic Cells
Kernicterus
Incidence
At first birth no harm
3% in second Rh-positive babies
10% in third Rh-positive babies
So on
Treatment
400 milliliters of Rh-Negative blood in 1.5 or more hours
6 or more weeks till Rh-negative blood is replaced by
infant’s own Rh-positive blood
Prevention
Anti-D- Antibody to 28- 30 weeks of gestation to
expectant mother or to mother who had delivered
Anti-D-Antibody causes
Inhibit antigen-induced B lymphocyte antibody
production
Attaches to D antigen sites on Rh-positive fetal red blood
cells
Acute Kidney Shut Down
RENAL VASOCONSTRICTION
CIRCULATORY SHOCK
RENAL TUBULAR BLOCKADGE due to precipitation
of hemoglobin
Transplantation
Autografts
Isografts
Allografts
Xenografts
Human leukocyte antigen
(HLA)
150 different HLA antigens
SIX of these are present on tissue cell membrane
TISSUE TYPING:
HLA on WBC
Tissue typing on membrane of lymphocytes
Best possible combination
Prevention of graft
rejection
T-cell is mainly responsible for graft rejection
Drugs to prevent graft rejection
1. Glucocorticoids
2. Azathioprine
3. Cyclosporine
Death due to unprotected body against the bacterial or viral
infections

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Blood types.....Arslan_Liaqat (fdc)

  • 2. Blood cells have 30 commonly antigens and more than 100 rare antigens Antigens are also called AGGLUTINOGENS Antibodies are also called AGGLUTININS which are mostly IgM and IgG Two major blood group system 1. O-A-B blood group system 2. Rh system
  • 3.
  • 4.
  • 5.
  • 6. Transfusion reaction Clumping of red blood cells as a result of mismatched blood groups is called as AGGLUTINATION IgG have 2 binding sites IgM have 10 binding sites ( HEMOLYSINS)
  • 7. Transfusion reaction Acute Reactions: 1.Agglutination: due to clumping 2.Hemolysis: due to lytic coplex of complement 3. Allergic reaction: Due to reaction with donors protein 4.Febrile Reaction: Due to pyrogens and wbc 5.Acute kidney shutdown: due to i. vasoconstrictions because of toxins ii.loss of recipient RBCs and because of toxins lead to vasodilation and increased permeability of vessels lead to circulatory shock iii. Tubular blockage because of heptoglobin consumption
  • 8. Delayed reactions Delayed hemolytic reactions: either physical rupture of clmped RBC or attack of WBC on clumbed RBC eads todelayed hemolysis and release of bilirubin,leads to jundice Air embolism: Bacterial contamination Iron Overload Ion changes: Hyperkalemia,Hypernatrimia ,Hypocalcemia Transfusion of disease :e.g Hepatitis Thrombophlebitis: due to faulty techniue
  • 9. Products of complement system cause rupture of donor RBCs & release of free Hb in the plasma. This is called the Immediate Response. Due to agglutination RBCs clog smaller blood vessels & further phagocytosis by macrophages causes further release of Hb & other toxins in the plasma. This is known as the Delayed Response.
  • 10. Transfusion reaction Mismatched blood group always causes agglutination of Donor red blood cells due to 1. Donor agglutinins are diluted by recipients plasma 2. Recipients agglutinins are not diluted by small amount of infused blood Jaundiced is seen when more than 400 milliliters of blood is hemolyzed in a day
  • 12. Rh blood type Six antigens or Rh factors C, D, E, c, d, e D antigen presence or absence give positive or negative blood group Delayed transfusion reaction Anti-Rh- Agglutinins develops in 2 to 4 weeks and reaches its maximum concentration 2 to 4 months later
  • 13. Erythroblastosis Fetalis Hemolytic disease of newborn Characterized by agglutination and Phagocytosis of fetus’s red blood cells Father Mother Fetus Rh +ve Rh-ve Rh+ve from father
  • 14.
  • 16. Incidence At first birth no harm 3% in second Rh-positive babies 10% in third Rh-positive babies So on
  • 17. Treatment 400 milliliters of Rh-Negative blood in 1.5 or more hours 6 or more weeks till Rh-negative blood is replaced by infant’s own Rh-positive blood
  • 18. Prevention Anti-D- Antibody to 28- 30 weeks of gestation to expectant mother or to mother who had delivered Anti-D-Antibody causes Inhibit antigen-induced B lymphocyte antibody production Attaches to D antigen sites on Rh-positive fetal red blood cells
  • 19.
  • 20. Acute Kidney Shut Down RENAL VASOCONSTRICTION CIRCULATORY SHOCK RENAL TUBULAR BLOCKADGE due to precipitation of hemoglobin
  • 22. Human leukocyte antigen (HLA) 150 different HLA antigens SIX of these are present on tissue cell membrane TISSUE TYPING: HLA on WBC Tissue typing on membrane of lymphocytes Best possible combination
  • 23. Prevention of graft rejection T-cell is mainly responsible for graft rejection Drugs to prevent graft rejection 1. Glucocorticoids 2. Azathioprine 3. Cyclosporine Death due to unprotected body against the bacterial or viral infections