Lecture 5 Flashcards
is required when testing donor bloods
Determining the D status of an RBC sample
All Rh-negative, weak D-negative obstetric patients are candidates for
Rh immune globulin (RhIg)
Rh immune globulin (RhIg)
a drug injected to prevent Rh-negative individuals exposed to Rh-positive RBC’s from developing anti-D
When can accurate Rh can’t be determined?
newborn cells are coated with maternal IgG anti-D in utero, very few D antigens
blocking phenomenon
Blocking phenomenon
An overabundance of antibodies is coating the red cell
take up all antigen sites on the cell
Most Rh antibodies are what?
IgG and react best at 37oC or after AHG
Rh antibodies are usually produced
after exposure, i.e.. Pregnancy or transfusion
greatest clinical significance
IgG1 and IgG3
Rh antibodies do not bind to what?
Complement
When Rh IgG crosses what, what happens?
The placenta
Results in positive DAT
erythroblastosis fetalis
Erythroblast released into circulation
Order of most to least Rh antigens
D>c>E>C>e
How immunogenic are Rh antigens?
highly immunogenic
Antibodies appear
120 days of a primary exposure
2 to 7 days of a secondary exposure
Rh-mediated hemolytic transfusion reactions, whether primary or secondary usually result in?
extravascular destruction of immunoglobulin coated cells
Reactions signs destruction of immunoglobulin coated cells
Fever, mild bilirubin elevation, decreased hemoglobin & haptoglobin
Hemolytic Disease of the Newborn
Occurs with D-negative women during pregnancy and following delivery of a D-positive fetus
What is given to pregnant mothers who are at risk of HDN
Rh-immune globulin
Rhnull syndrome
Individuals who lack all Rh antigens on their RBC’s
produced by two different genetic mechanisms: Regular and Amorphic type
Rhnull syndrome: Regular type
a mutation in the RHAG gene
Results in no Rh polypeptides or RHAG antigen expression
Rhnull syndrome: Amorphic type
there is a mutation in each of the RHCE genes and a deletion of the RHD gene
individuals with Rhnull syndrome can only get
only Rhnull blood can be given
Rhmod phenotype
partial suppression of Rh gene expression and exhibit features similar to those with Rhnull syndrome; clinical symptoms are less severe
High-frequency antigen
antigen whose frequency in the population is 98% to 99%.
Aka high-incidence antigen
Low-frequency antigen
antigen whose frequency in a random population is very low - < 0%.
Aka low-incidence antigen
Cw Phenotypes
antithetical to the high-incidence antigen MAR
F phenotype
ce genes expressed
expressed on the RBC when both c and e are present on the same haplotype (cis position)
Anti-F
reported to cause HDN and Transfusion reactions
Rhi
Expressed as Ce
present when C and e are in the cis configuration (Like F)
Parts of D mosaic
Rh:13, Rh:14, Rh:15, Rh:16
Rh:23, Rh:30, Rh:40
all low-frequency antigens associated with a specific category of partial-D
Rh0
present on all RBCs with common Rh phenotypes (R1R1, R2R2, rr)
e Variants
Appears especially in the black population
e antigen may exhibit the same mosaic quality described for D
recognized when they make antibodies that behave as anti-e
Deletions
very uncommon phenotypes that demonstrate no Cc and/or Ee reactivity
often have an unusual strong D
LW Antigen is similar to
Rh systems
LW Antigen reacts
strongly with most D-positive RBCs
weakly (sometimes not at all) with Rh-negative RBCs
never with Rhnull cells
When was LW antigen discovered?
with the beginning of Rh antigen recognition
Experiment with Rhesus monkey
Lw Antigen alleles
Lwa
LWb
LW ( a silent allele)
express no LW on the RBC
Persons lacking LW altogether are LW/LW
Which LW genes are common and which is rare
LWa is very common
LWb is rare
When the Rhnull is present
Rh and LW genes are not expressed on the RBC
Anti-LW usually reacts more strongly
with D-positive RBCs than with D-negative adult RBCs
weak anti-LW may react only
With D-positive RBCs
How can weak anti-LW react with D-negative adult RBCs
enhanced techniques may be required to demonstrate its reactivity with D-negative cells
