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BII > L17: Introduction to blood group serology > Flashcards

L17: Introduction to blood group serology Flashcards

1
Q

Blood group antigens

A
  • Glycoproteins and glycolipids present on surface of red cells
  • Some e.g. ABO present more widely on endothelial surfaces
  • Genetically determined: generally autosomal and co-dominant (exception - Xg system sex-linked)
  • Limited understanding of biological function
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2
Q

Genetic control of blood groups

A

Protein determinants: gene codes for antigenic determinant itself - Rh, Kell, Duffy, Kidd systems
Glycolipid determinants: gene codes for production of enzymes that add/remove carbohydrate or lipids - ABO, Lewis group systems

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3
Q

Functional aspects of antigens

A

Duffy blood group system and malaria:

  • Duffy antigen acts as entry point to red cell for malarial parasite
  • Fya-negative Fyb-negative up to 40% of black Africans (natural selection for malarial resistance)
  • Fya-Fyb- phenotype is rare in Caucasians

McLeod phenotype:
- Kx null phenotype associated with chronic granulomatous disease and acanthocytosis

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4
Q

Blood groups and populations

A
  • Distribution likely due to genetic drift
  • No biological advantage apparent
  • Clinical impact in relation to compatibility
    e. g. more caucasians than polynesians Rh-negative or MNS system (U phenotype) only present in black African population
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5
Q

Blood group antibodies

A
  • Blood group systems important because of their ability to stimulate antibody production
  • ABs recognise ‘foreign’ antigens
  • May be IgM, IgG, IgA
  • Naturally occurring or immune stimulated
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6
Q

Naturally occurring red cell antibodies

A
  • Develop in absence of exposure to red cell antigens
  • Stimulated by cross-reacting antigens derived from bacteria
  • Not present at birth, develop in first yr of life
  • Usually related to lipid antigens
  • Significant IgM component (some IgG)
  • ABO and Lewis antigens in this category
  • Can activate complement and red cell destruction is intravascular
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7
Q

Immune stimulated red cell antibodies

A
  • Develop only after exposure to specific antigens
  • Transfusion, pregnancy, injection
  • Normally IgG
  • Cannot activate complement (or only early phase) and red cell destruction is extravascular
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8
Q

ABO antigens

A
  • ABO antigens widely distributed: blood cells, epithelial cells, body fluids
  • Phenotype determined by a series of glycosyltransferase enzymes (add carbohydrates to basic membrane structure)
  • H antigen necessary for ABO phenotype to be expressed
  • Antibodies to expressed phenotype appear in first 3-6mths
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9
Q

Specific ABO phenotypes (terminal sugars)

A 
A = terminal sugar is N acetyl galactosamine 
B = D galactose 
O = nil
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10
Q

ABO system

A

OO genotype: O phenotype, anti-A and anti-B antibodies, 46.5% in NZ
AA, AO: A, anti-B antibodies, 40% in NZ
BB, BO: B, anti-A antibodies, 9% in NZ
AB: AB, nil antibodies, 4.5% in NZ

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11
Q

Clinical relevance of ABO system

A
  • Most important blood group system, transfusion errors can be fatal
    ABO incompatible transfusion results in complement activation leading to:
  • Intravascular haemolysis
  • Renal failure
  • Disseminated intravascular coagulation
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12
Q

ABO transfusion - suitable donors

A

Recipient O: anti-A and anti-B antibodies
–> acceptable donor is O (universal donor)

Recipient A: anti-B antibodies
–> acceptable donor A or O

Recipient B: anti-A antibodies
–> acceptable donor B or O

Recipient AB (universal recipient): no ABs
--> AB, A, B, O
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13
Q

Rh blood group system

A
  • 2nd most important system
  • Protein determinant
  • Expression only on red blood cells
  • Antibodies produced following immune stimulation
    Highly immunogenic, esp. Rh(D)
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14
Q

Rh(D) antigen

A
  • Most important antigen of Rh system
  • All individuals Rh(D) positive or negative
  • DD or Dd = Rh(D) positive
  • dd = Rh(D) negative
  • d antigen is an amorph
  • Difference in frequency between populations
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15
Q

Rh(D) and transfusion

A
  • 90% of Rh(D) negative people transfused with Rh(d) positive red cells will develop anti-D
  • Anti-D = IgG antibody unable to bind complement, red cell destruction extravascular
  • Anti-D most common cause of haemolytic disease of newborn
  • Normally transfuse red cells of same Rh(D) type as recipient
  • Never transfuse Rh(D) pos red cells to an Rh(D) neg female of child-bearing age
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16
Q

Expanded Rh system

A
  • Rh antigen is product of 3 genetically closely linked alleles: C, c, D, d, E, e
  • Can use expanded system in family studies and donor searches
17
Q

Minor blood group systems

A
  • Over 400 defined, majority only theoretical interest
  • Clinical importance varies (freq of antigen in population, freq of AB production following transfusion, ability of AB to destroy transfused red cells)
  • Kell, Kidd, Duffy
18
Q

Laboratory techniques

A
  • Routine testing: detection of antigens and antibodies using agglutination technique
  • Antigen testing usually uses commercially sources monoclonal reagents
  • Molecular typing methods (increasing)
19
Q

Agglutination methods

A
  • Red cells negatively charged = zeta potential
  • IgM (pentamer) larger than zeta potential so can produce cross-linking -> agglutination
  • IgG (monomer) too small to produce cross-linking so potentiator needed (anti-human globulin)
20
Q

Haemolytic disease of the newborn

A
  • Occurs when maternal ABs cross placenta
  • -> destruction of fetal cells
  • Always involves IgG antibodies
  • Greatly reduced by immunoprophylaxis
21
Q

Mechanism of haemolytic disease of newborn

A
  • Most frequently caused by presence of anti-D (then anti-c and anti-Kell)
  • Infant Rh(D) positive and mother Rh(D) negative
  • Fetal red cells can enter maternal circulation (esp. during 3rd trimester and delivery e.g. feto-maternal haemorrhage)
  • Mother than develops anti-D
  • Next pregnancy: anti-D crosses placenta and results in damage to fetal red cells
22
Q

Consequences of haemolytic disease of newborn

A
  • Can cause fetal anaemia, cardiac failure –> hydrops fetalis (congestive heart failure)
  • More commonly survives pregnancy –> becomes jaundiced (in utero bilirubin removed by maternal circulation) –> bilirubin can cross BBB and cause kernicterus (neurological abnormalities e.g. cerebral palsy)
23
Q

Prevention of Rh(D) haemolytic disease of newborn

A
  • Anti-D immunoglobulin given routinely after birth of Rh(D) pos baby to Rh(D) neg mother
  • Give standard post-natal dose 625 IU
  • Kliehauer test to detect women with larger fetomaternal bleeds (larger dose may be req)
  • Anti-D immunoglobulin also given after e.g. abortion, termination, amniocentesis
24
Q

ABO haemolytic disease of newborn

A
  • ABO incompatibility between mother and fetus is common
  • Significant ABO haemolytic disease is rare: (AB antigens weakly expressed in fetus and newborn, widely distributed in placental tissues and absorb antibodies before reaching fetus)
  • ABO HDN mild and transfusion rarely req

BII (41 decks)

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