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MLSCI 475 > Platelet Allo-Antigens > Flashcards

Platelet Allo-Antigens Flashcards

1
Q

surface receptors and antigens on platelets

A

HPA (human platelet allo-antigens)
class I HLA
ABO

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2
Q

T or F. HP1b is more common than HP1a

A

F! “a” is more common/frequent

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3
Q

methods used to detect HPA antibodies

A

Luminex
- PakLX assay
among others

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4
Q

treatment of FNAIT

A

transfusion with maternal washed PLTS - preferably apheresis or compatible PLTs is antibody specificity unknown

unrelated HPA typed donors are often used
> randome PLT units may result in successful increments

percutaneous umbilical blood sampling (PUBS) can be performed to monitor PLT count in utero (and transfuse)

treatment of mom with IVIg during pregnancy
> IVIg therapy in baby has had mixed success

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5
Q

treatment of PTP

A

IVIg
corticosteroids
platelet transfusion
> transfusion of HPA compatible platelts when possible
plasmapheresis
in future, use of HPA matched units and IVIg pre-transfusion

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6
Q

GPIIb/IIIa

A

when activated, binds natural ligands and causes aggregation
= fibrinogen, Vitronectin, fibronectin, vWF

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7
Q

HPA alloantigens on both GPIIb/IIIa subunits that are screened for in Ab tests

A
  • GPIIb = HPA-3
  • GPIIIa = HPA-1,-4
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8
Q

this binds collagen and takes part in adhesion + activation

A

GPIa/IIa

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9
Q

HPA ALLOANIGENS ON GP1A ONLY

A

HPA-5

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10
Q

vWF receptor

A

GP1b/V/IX

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11
Q

how do antibodies to non-self platelet antigens develop?

A

after exposure to non-self platelet HPA following transfusion and pregnancy

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12
Q

what is FNAIT

A

fetal/neonatal allo-immune thrombocytopenia
- mom develops IgG Abs to baby’s plt allo-antigens
- passive thrombocytopenia (can occur in utero)

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13
Q

T or F. FNAIT occurs in first pregnancy

A

T

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14
Q

T or F. FNAIT is self-resolving

A

once baby is born, source of Abs (mom) is cut off
- thrombocytopenia 1-3 wks post-partum

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15
Q

lab detection of HPA Abs in FNAIT

A
  • Ab screen in maternal serum
    > during gestation if previous pregnancy was affected
  • HPA alloantigen typing of mom and dad
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16
Q

most common HPA antibody detected

A

anti HPA-1a

17
Q

T or F. FNAIT lab detection is quantitative

A

F! Ab screen not quant but different sample dates can be tested in parallel for estimate of titre changes

18
Q

methods for HPA Ab detection

A

platelet immunofluorescence (PIFT-FFC); read by flow

solid phase adherence assay (SPAA)

antigen capture ELISA (ACE)

monoclonal antibody-specific immobilization of platelet antigens (MAIPA)

Luminex (PakLX assay)

19
Q

describe the Luminex screening/ID test

A
  • uses phycoerythrin (PE) labelled anti-human IgG to detect antibodies bound to plt antigens on the beads
  • amt of fluorescence detected (MFI) determines whether bead is + or -
  • which Abs are present is determined by combination of beads that are reacting in the panel
20
Q

what is the follow up done to antibody ID Testing?

A

HPA genotyping
> LinkSeq HPA typing kits (qPCR)

if HLA class I detected = Ab specificity and typing

21
Q

describe HPA typing by qPCR

A
  • specific DNa sequences amplified while also being quantified by spectrofluorimetric methods
    => Sybr Green = dsDNA binding fluorescent molecule
  • amplified product is then heated to identify melt curve characteristics that determine the presence/absence of HPA antigen
22
Q

PTP

A

post transfusion purpura
- are event = acute episode of severe immune thrombocytopenia after ~1wk post-transfusion
- amnestic response to previous exposure to platelet allo-antigens

23
Q

T or F. PTP more frequent in adults

A

T, more in females

24
Q

T or F. PTP is self-resolving

A

T, but can be fatal

25
Q

PLT counts in PTP

A
  • pt’s own plts and transfused plts are destroyed so <15 plt count
  • unknown mechanism
    > immune complexes clearing all plts from circulation?
    > auto Abs?
26
Q

lab tests for PTP

A
  • Luminex screening/ID test (same for HPA alloAbs)
  • use serum from pt
  • anti-HPA1a most common
  • if required = HLA genotyping and HLA Ab specificity and typing
27
Q

PLTRE

A

plt transfusion refractoriness = a repeated suboptimal response to platelet transfusions with lower-than-expected posttransfusion count increments
- most common = anti HLA Class I; some due to anti-HPA

28
Q

often, it is recommended to have at least ____ episodes of unsatisfactory plt increment before refractoriness is investigates

A

two

29
Q

correct count increment or CCI used for plt increment assessments

A

[post-transfusion - pre-transfusion plt count/uL x body SA (m2)] /
number of plts in component x 10^-11

30
Q

altnernate cause of thrombocytopenia

A

fever
splenomegaly
DIC
drug-related immune destruction (quinidine, penicillin, etc.)

31
Q

testing for PLT refractoriness

A
  1. class I HLA Ab screen
    = if none …
  2. HPA Ab
  3. HLA typing if required
  4. HPA genotyping if required
32
Q

treatment of PTR

A
  • use HLA matched units
  • IVIg??? = studies vary
  • continuous monitoring of PRA following future transfusions
33
Q

this antigen is not well expressed on PLTs

A

C

34
Q

guidelines for PLT transfusion

A
  1. matching for plt donor HLA-A/B antigens
  2. provide plts that lack Ag pt has antibody to
  3. substitute cross-reactive units if antigen matched not available
  4. matching for C not necessary
  5. mismatching for weakly expressed (ex: B44, B45)
  6. ABO expressed on plts BUT ABO matching usually not critical but should be considered if HLA matched are not effective
35
Q

methods for HLA Ab testing in refractory pts

A
  • serology: CDC/CDC-AHG
  • solif phase assays:

MLSCI 475 (22 decks)

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