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Transfusion Medicine Fellowship > Platelets & Granulocytes > Flashcards

Platelets & Granulocytes Flashcards

1
Q

What antigens are expressed in platelets?

A

ABH, HLA, HPAs (significant), also I/P/Lewis and Cromer (insignificant)

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2
Q

What HPAs are located on GpIIb/IIIa (CD41/61)?

A

HPA-1
HPA-3
HPA-4

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3
Q

What is the most important HPA and what is its frequency?

A

HPA-1A/B. AA (72%), AB (26%), BB (2%)

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4
Q

What HPAs are located on GP1b/V/IX (CD42)?

A

HPA-2

HPA-12

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5
Q

What is the number 2 cause of NAIT?

A

Anti-HPA-5a antibodies, found on GpIa/IIa (a collagen receptor).

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6
Q

Where are ABH carried on platelets?

A

On GpIIb and PECAM-1/CD31. Note that A2 patients express so little A their platelets are effectively group O.

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7
Q

Recall some minor platelet antigens.

A

CD109 (houses HPA-15)
GPIV/CD36
GPVI

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8
Q

What size pool is needed to adequately find HLA-matched donors? What matches are best?

A

1000-3000 donors. A, B1X, B1U, B2UX are acceptable (no mismatches, cross-reactivity OK).

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9
Q

What is antibody specificity prediction (ASP)?

A

Giving platelets with HLA antigens against which there are no known antibodies (despite being non-identical).

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10
Q

How is platelet crossmatching performed

A

Solid phase red cell assay (SPRCA)

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11
Q

How is FNAIT tested for? How rapidly can it develop?

A

Test maternal serum for antibodies and genotype father. Can develop intra-pregnancy.

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12
Q

What drugs can cause thrombocytopenia?

A

Sulfas, quinine, vancomycin, HEPARIN, GpIIb/IIIa antagonists.

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13
Q

Why are platelets in HIT activated?

A

The anti-PF4 antibodies cawn also activate plt FcyRIIa.

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14
Q

What testing methods exist to identify platelet antigens/antibodies?

A

Glycoprotein-specific assays (antigen captures, ACE/MACE/MAIPA)

Whole platelet assays (SPRCA, flow cytometry)

Genotyping

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15
Q

How is testing in ITP done?

A

First of all, it’s not always necessary. But most tests look at eluates from platelets for specificity against platelet glycoprotein antigens.

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16
Q

Granulocyte antigen-antibody interactions are implicated in what conditions?

A 
Neonatal alloimmune neutropenia (NAN)
TRALI
FNHTRs
Autoimmune neutropenias (AIN)
Granulocyte refractoriness
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17
Q

What is HNA-1 located on?

A

FcyRIIIb (CD16b, 100-200k copies per cell)

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18
Q

What is CD177?

A

Some surface marker only notable for housing HNA-2. Up to 11% of patients are null and can develop antibodies.

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19
Q

What is the most important HNA antigen? Where is it located?

A

HNA-3, located on CTL3.

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20
Q

What HNAs are housed in CD11?

A

HNA-4 (CD11b/18)

HNA-5 (CD11a/18)

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21
Q

What blood group antigens are on neutrophils?

A

NOT ABO/RH

MHC-I/II

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22
Q

Neonatal alloimmune neutropenia

A

Maternal alloimmune response against fetal HNA-1a, -1b, -2, or others. Can be life threatening, treated with antibiotics, IVIG, G-CSF and PLEX

23
Q

How is granulocyte testing performed?

A

Very difficultly, because of shortgevity of cells and interference of HLA antibodies.

24
Q

What granulocyte tests exist?

A

Granulocyte agglutination test (pt serum + granulocyte)
Immunofluorescence (wash neutrophils, add fluoro-AHG)
Luminex
HNA typing (genotypic)

25
Q

How frequently are platelet units bacterially contaminated? How often do they cause serious reactions? Fatal reactions?

A

About 1 in 1000-3000. Only about 1 in 6 of these will cause any reaction, and even fewer will cause serious reactions. Perhaps 0.5-1 in a million are fatal.

26
Q

What organisms most often cause fatal septic platelet transfusion reactions?

A

Gram-negative rods! GPCs are more common but these are generally not fatal.

27
Q

How can bacterial contamination of platelets be avoided?

A

Use screening questions and temperature. Clean the site thoroughly and divert the first portion of the draw (doesn’t stop GNR bacteremia). Use single donor packs, not pools.

28
Q

What are the main bacterial platelet contamination detection methods currently in use?

A

BacT/ALERT: 4-8mL in aerobic+anaerobic bottle. Colorimetric CO2 detection.
Pall eBDS: 2-3mL in a bag with tryptic soy broth. Measure oxygen consumption (misses anaerobes).

29
Q

How can bacterial contamination in platelets be reduced or inhibited?

A

Cold storage

Pathogen-reduction (INTERCEPT, Mirasol, Theraflex) - Amotosalen, riboflavin, potassium/magnesium?

30
Q

How are granulocyte donors primed? What are the side effects?

A

G-CSF (newer) and/or steroids, either generally given about 12 hours ahead of harvest. Musculoskeletal pain is common. Long-term effects are not well described.

31
Q

What are the classes of platelet HLA matching?

A

A (4 loci matched)
BU (3 loci matched–homozygous for one)
BX (3 loci matched, 1 CREG)
C/D/R (mismatched)

32
Q

What disease states leave patients at very high risk of alloimmunization against HPAs?

A

Glanzmann’s thrombasthenia, Bernard-Soulier (congenital absence of these antigens)

33
Q

What is the cause of FNAIT? Any associations?

A

Maternal anti-HLA-1a (or 4b) antibodies causing isolated fetal thrombocytopenia. Penetrance is associated with HLA-DRB3*01.

34
Q

Post-transfusion purpura

A

Mostly seen in women who have anti-HPA-1a antibodies. Can be fatal. Requires positive serology to diagnose. Treated with steroids/IVIG and maybe TPE.

35
Q

What is “reverse PTP”?

A

Thrombocytopenia resulting from transfusion of a plasma-rich product from an HPA-1a-immunized patient (usually pregnant women; downtrending along with TRALI).

36
Q

What is the full half-life of a platelet in vivo?

A

10.5d

37
Q

At what pH should platelets be kept above?

A

6.2 (below, platelets agglutinate and lyse)

38
Q

What are the platelet bags made of? Why?

A

PVC, plus plasticizers such as DEHP. Must be gas-permeable.

39
Q

What is the required count for apheresis platelets?

A

> 3 x 10^11 in at least 75% (90%?) of units

40
Q

How many red cells can contaminate a platelet before RHD alloimmunization is a concern?

A

0.03mL of red cells; above this give RhoGAM. This is less than the amount expected in apheresis (0.001mL)

41
Q

What percentage of alloimmunized patients are refractory?

A

Only 30%

42
Q

What HPA is especially associated with platelet refractoriness?

A

GPIV (absent in many African americans, anti-GPIV antibodies cause refractoriness)

43
Q

List HLA platelet matches by effectiveness.

A

A > B1U > B2U > B1X > B2UX > B2X > C,D

44
Q

Time to peak granulocyte mobilization

A

8-16 hours (average 12) using a G-CSF/steroid regimen.

45
Q

What is the usual red cell content of a granulocyte unit?

A

~30mL RBCs (~10% hematocrit)

46
Q

How does lack of IDM test resulting get resolved?

A

Select repeat donors who have had IDMs in last 30 days

Extend results and release at medical director discretion

47
Q

During granulocyte collection, how much blood is processed, and for how long?

A

It is a typical apheresis procedure, processing 7-10L WB and taking about 100min on average.

48
Q

What are the consequences of HES use?

A

Possible anaphylactic or flu-like reactions.

Decreased von willebrand factor and increased aPTT

49
Q

What are pooled granulocytes?

A

A product made from whole blood using buffy coats, only used in Europe, not the US.

50
Q

What is the required count for granulocyte?

A

Minimum 1 x 10^10 granulocytes in at least 75% of units.

51
Q

From where can PRP be sourced? How is it collected?

A

Autologous or allogeneic. Dozens of collection methods with hetereogeneous and crappy literature. Note that some products may contain thrombin as a platelet activator.

52
Q

What is the rationale behind therapeutic PRP?

A

Platelets carry chemokines which promote wound healing by stimulating mesenchymal and endothelial proliferation and angiogenesis.

53
Q

What different types of PRP products exist?

A

Pure PRP
Leuko-rich PRP
Plt-rich fibrin (stronger clot and gel matrix)
Leuko- and plt-rich fibrin

54
Q

What is the evidence in support of PRP?

A

Scant. Most injury settings derive some pain benefit but do not show faster return to function.

Transfusion Medicine Fellowship (34 decks)

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