Blood grouping

52,568 views

Published on

AGA KHAN UNIVERSITY HOSPITAL

Published in: Education, Business, Technology
1 Comment
91 Likes
Statistics
Notes
  • Hi All, We are planning to start Hadoop online training batch on this week... If any one interested to attend the demo please register in our website... For this batch we are also provide everyday recorded sessions with Materials. For more information feel free to contact us : siva@keylabstraining.com. For Course Content and Recorded Demo Click Here : http://www.keylabstraining.com/hadoop-online-training-hyderabad-bangalore
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Views
Total views
52,568
On SlideShare
0
From Embeds
0
Number of Embeds
152
Actions
Shares
0
Downloads
2,102
Comments
1
Likes
91
Embeds 0
No embeds

No notes for slide

Blood grouping

  1. 1. BloodGrouping
  2. 2. History - Karl Landsteiner  Discovered the ABO Blood Group System in 1901  He and his five co-workers began mixing each others red cells and serum together and inadvertently performed the first forward and reverse ABO groupings
  3. 3. Landsteiners Rule  If an antigen (Ag) is present on a patients red blood cells the corresponding antibody (Ab) will NOT be present in the patients plasma, under ‘normal conditions’.
  4. 4. MajorABO BloodGroup ABO Group Antigen Present Antigen Missing Antibody Present A A B Anti-B B B A Anti-A O None A and B Anti-A&B AB A and B None None
  5. 5. ABO Basics  Blood group antigens are actually sugars attached to the red blood cell.  Antigens are “built” onto the red cell.  Individuals inherit a gene which codes for specific sugar(s) to be added to the red cell.  The type of sugar added determines the blood group
  6. 6. Principle of blood grouping There are two principles 1-almost all normal healthy individuals above 3-6 months of age have “ naturally occurring Abs” to the ABO Ags that they lack These Abs termed naturally occurring because they were thought to arise without antigenic stimulation
  7. 7. Principle of blood grouping 2- These “naturally occurring” Abs are mostly IgM class. That means that, they are Abs capable of agglutinating saline/ low protein suspended red cell without enhancement and may activate complement cascade.
  8. 8. ABO and H Antigen Genetics  Genes at three separate loci control the occurrence and location of ABO antigens  The presence or absence of the A, B, and H antigens is controlled by the H and ABO genes
  9. 9. Location  The presence or absence of the ABH antigens on the red blood cell membrane is controlled by the H gene  The presence or absence of the ABH antigens in secretions is indirectly controlled by the Se gene
  10. 10. HAntigen  The H gene codes for an enzyme that adds the sugar fucose to the terminal sugar of a precursor substance (PS)  The precursor substance (proteins and lipids) is formed on an oligosaccharide chain (the basic structure)
  11. 11. RBC Precursor Structure Glucose Galactose N-acetylglucosamine Galactose Precursor Substance (stays the same) RBC
  12. 12. Formation of the H antigen Glucose Galactose N-acetylglucosamine Galactose Precursor Substance (stays the same) RBC H antigen Fucose
  13. 13. H antigen  The H antigen is the foundation upon which A and B antigens are built  A and B genes code for enzymes that add an immunodominant sugar to the H antigen  Immunodominant sugars are present at the terminal ends of the chains and confer the ABO antigen specificity
  14. 14. A and B Antigen  The “A” gene codes for an enzyme (transferase) that adds N-acetylgalactosamine to the terminal sugar of the H antigen  N-acetylgalactosaminyltransferase  The “B” gene codes for an enzyme that adds D- galactose to the terminal sugar of the H antigen  D-galactosyltransferase
  15. 15. Formation of theA antigen Glucose Galactose N-acetylglucosamine Galactose RBC Fucose N-acetylgalactosamine A antigen
  16. 16. Formation of the B antigen Glucose Galactose N-acetylglucosamine Galactose RBC Fucose Galactose B antigen
  17. 17. H antigen  Certain blood types possess more H antigen than others: O>A2>B>A2B>A1>A1B
  18. 18. Why do Group O individuals have more H antigen than the other groups? Group O individuals have no A or B genes to convert the H antigen to A or B antigens….that means more H antigen sites
  19. 19. Group O Group A Many H antigen sites Fewer H antigen sites A A A AA Most of the H antigen sites in a Group A individual have been converted to the A antigen
  20. 20. Genetics  The H antigen is found on the RBC when you have the Hh or HH genotype, but NOT from the hh genotype  The A antigen is found on the RBC when you have the Hh, HH, and A/A, A/O, orA/B genotypes  The B antigen is found on the RBC when you have the Hh, HH, and B/B, B/O, orA/B genotypes
  21. 21. Bombay Phenotype (Oh)  Inheritance of hh  The h gene is an amorph and results in little or no production of L-fucosyltransferase  Originally found in Bombay  Very rare (130 worldwide)
  22. 22. Bombay Phenotype (Oh)  The hh causes NO H antigen to be produced  Results in RBCs with no H, A, or B antigen (patient types as O)  Bombay RBCs are NOT agglutinated with anti-A, anti- B, or anti-H (no antigens present)  Bombay serum has strong anti-A, anti-B and anti- H, agglutinating ALL ABO blood groups  What bloodABO blood group would you use to transfuse this patient?? Another Bombay Group O RBCs cannot be given because they still have the H antigen You have to transfuse the patient with blood that contains NO H antigen
  23. 23. ABO antibodies  GroupA serum contains anti-B  Group B serum contains anti-A  GroupAB serum contains no antibodies  GroupO serum contains anti-A, anti-B, and anti-A,B
  24. 24. ABO antibodies  IgM is the predominant antibody in GroupA and Group B individuals  Anti-A  Anti-B  IgG (with some IgM) is the predominant antibody in GroupO individuals  Anti-A,B (with some anti-A and anti-B)
  25. 25. ABO antibodies  Reactions phase: Room temperature  Complement can be activated with ABO antibodies (mostly IgM, some IgG)  High titer: react strongly (4+)  Usually present within the first 3-6 months of life  Stable by ages 5-6 years  Decline in older age  Newborns may passively acquire maternal antibodies (IgG crosses placenta)  Reverse grouping (with serum) should not be performed on newborns or cord blood
  26. 26. ABO routine testing  Several methods for testing the ABO group of an individual exist.The most common method is:  Serology: This is a direct detection of the ABO antigens. It is the main method used in blood transfusion centres and hospital blood banks.  This form of testing involves two components: a)Antibodies that are specific at detecting a particular ABO antigen on RBCs.  b) Cells that are of a known ABO group that are agglutinated by the naturally occurring antibodies in the person's serum.
  27. 27. ABO ROUTINE TESTING DIRECT OR FORWARD GROUPING Test for antigens • Patient’s cells containing unknown antigens tested with known antisera • Antisera manufactured from human sera Aantisera used: Antisera Color Source Anti-A Blue Group B donor Anti-B Yellow Group A donor Anti-A,B Red Group O donor
  28. 28. Forward Grouping  Reaction of patient red blood cells tested with Reagent anti-A and anti-B antisera  Slide: 20-40% RBC suspension + anti-serum  Tube (12x75mm): 2-5% RBC suspension + anti-serum (centrifuge before read)
  29. 29. Forward Grouping Reaction Patterns for ABO Groups Blood group Agglutination with Anti-A Agglutination with Anti-B A + - B - + AB + + O - -
  30. 30. Reverse grouping • serum is combined with cells having known Ag content in a 2:1 ratio • uses commercially prepared reagents containing saline-suspended A1 and B cells
  31. 31. Reverse grouping Reaction Patterns for ABO Groups Blood Group Agglutination with A cells Agglutination with B cells A - + B + - AB - - O + +
  32. 32.  Grading of Agglutination: Negative (0) No clumps or aggregates Weak (+/-) Tiny clumps or aggregates barely visible macroscopically or to the naked eye 1+ Few small aggregates visible macroscopically 2+ Medium-sized aggregates 3+ Several large aggregates 4+ One solid aggregate
  33. 33. ABO blood group (forward blood grouping) Patient Red CellsTested With InterpretationAnti-BAnti-APatient 001 04+2 4+03 4+4+4
  34. 34. ABO blood group (forward blood grouping) Patient Red CellsTested With InterpretationAnti-BAnti-APatient O001 A04+2 B4+03 AB4+4+4
  35. 35. Reverse Grouping (Confirmatory grouping Patient SERUMTestedWith InterpretationB CellsA1 CellsPatient 4+4+1 4+02 04+3 004
  36. 36. Reverse Grouping (Confirmatory grouping Patient SERUMTestedWith InterpretationB CellsA1 CellsPatient O4+4+1 A4+02 B04+3 AB004
  37. 37. Forward & reverse ABO blood grouping Reaction of CellsTested With Reaction of SerumTested Against ABO Group Anti-A Anti-B A1 Cells B Cells 1 0 0 + + O 2 + 0 0 + A 3 0 + + 0 B 4 + + 0 0 AB
  38. 38. Forward & reverse ABO blood grouping Reaction of CellsTested With Reaction of SerumTested Against ABO Group Anti-A Anti-B A1 Cells B Cells 1 0 0 + + 2 + 0 0 + 3 0 + + 0 4 + + 0 0
  39. 39. ID card system  This ID-Card contains a mixture of human polyclonal and monoclonal anti-A, human polyclonal anti-B and human polyclonal anti-D antibodies.  The microtube ctl is the negative control.Two microtubes with neutral gel serve for reverse grouping with A1 and B cells.
  40. 40.  Fully-automatic walk-away for ID-Cards  Stand alone instrument  Continuous sample loading  Continuous reagent loading  Priority samples (STAT)  Reagent stock  High throughput
  41. 41.  Optimized for small blood volumes  Dispense verification  Easy-to-use  Full test menu  Wi-Fi  Touchscreen 17"  Host connectivity  Internal & external validation  Capacity 180 samples 240 ID-Cards 28 reagent vials
  42. 42. Thank you….

×