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4.2 Blood Transfusion Science > Platelet Serology and Transfusion > Flashcards

Platelet Serology and Transfusion Flashcards

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1
Q

What patient cohort is most likely to get platelet transfusion

A

Leukaemia patients

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2
Q

What platelet count would you be concerned with

A

Less than 150 if not a leukamia patient

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3
Q

Why are leukaemia patients so highly transfused with platelets

A

Their counts tend to not or barely improve after transfusion, will need multiple tranfusions to increase prior to surgery etc

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4
Q

What antigens are found on platelets

A

ABO (5-10%) high expression of A or B

HLA class I

HPA antigens

Lewis, I, P, Cromer, DAF

If LD they will have less class II due to less leucocytes

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5
Q

Why do we universally irradiate platelets?

A

To prevent GVHD

This doesnt affect platelets unlike rbcs

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6
Q

Are platelets typed

A

Yes as though to be a rbc product

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7
Q

What kind of antigens are found on platelets

A

Cold, carbohydrate antigens

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8
Q

Talk about HPAs, what are they, how were they discovered

A

Human platelet antigens

We dont know the number of these antigens

First discovered in investigation of NAIT

Located on platelet membrane glycoproteins

These GPs are involved in haemostasis, through integrated with proteins in the endothelium and coagulation proteins

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9
Q

How were HPAs originall named

A

They were originally named after antibody markers

There is a lot of overlap between groups

ISBT established HPA nomenclature in 1990

Systems are bi-alleleic with each allele being co-dominant

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10
Q

How are HPAs named, what is the significance of this

A

Each system numbered consecutively: HPA1, HPA2 etc

High frequency antigens = a, low = b etc

Thus any a antigens are hard to get platelets for

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11
Q

What are the most frequently detected antibodies

A

anti-HPA-1a

anti-HPA-5b

anti-HPA-15b

NB: 1a and 5b most associated with neonates

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12
Q

Where is HLA typing done?

A

Bristol

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13
Q

What are the three roles of different platelet antigens?

A

Collagen binding

Fibrinogen binding

vWF binding

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14
Q

When might you see antibodies against HPA

A

In certain conditions where there are issues with poor binding to collagen or fibrinogen etc -> they will lack certain HPA antigens and thus produce antibodies against them

These can be hard to get platelets for

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15
Q

Where are the majority of HPAs located

A

On the GpIIb/IIIa complex

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16
Q

What is the role of GpIIb/IIIa complex?

A

Central role in platelet aggregation

Role as a receptor for fibrinogen and fibronectin

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17
Q

List some of the platelet membrane glycoprotein complexes

A

GpIIb/IIa

Gp Ib/IX/V

GP Ia/IIa

GP IV

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18
Q

Talk about GP Ib/IX/V

A

Receptor for vWF

deficient in Bernard-Soulier syndrome

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19
Q

Talk about GP Ia/IIa

A

Involved in adhesion to collagen

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20
Q

In who is GPIIb/IIIa deficient in

A

Deficient in Glanzmann’s Thrombasthenia

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21
Q

In who is GP IV deficient in?

A

3-5% of Black and Asian individuals

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22
Q

What are the different platelet products

A

Pooled platelets

Apheresis platelets

NB: all are irradiated

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23
Q

How are pooled platelets made

A

Made from top and bottom packs

Platelet rich plasma/buffy coat of four donations are pooled together

If one unit is Rh+ then whole pool is Rh+

Platelet additive solution

LD, Irradiated and BacT

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24
Q

What is the conc of apheresis vs pooled platelets

A

45-85 x 10^9 pooled

3.0 x 10^11 apheresis

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25
How are platelets stored
@22 degrees Maintained pH of 6 or above
26
What is the ratio of PAS to palsma in pooled units
75% PAS and 25% plasma
27
What donors do we use for plasma and why?
Male only No HLA antibodies Avoid Trali
28
Since when have we been irradiating platelets and why?
Since 1998 Reduce FNHTR Reduce refractoriness
29
Talk about apheresis donation
Takes 60-90 minutes Can donate every 28 days Can donate up to 3 splits at once Platelets are removed and other components are returned to the donor LD as part of process Storage as per pooled platelets but in plasma not PAS
30
What are some alternatives to PAS
Electrolyte solutions containing acetate, citrate, phosphate and chloride
31
For how long are platelets stored and in what
Constant controlled agitation with gaseous exchange Polyolefin packs 7 day storage (used to be 5 days)
32
When are platelets indicated?
Haemorrhage prophylaxis in thrombocytopenia or platelet function defects e.g. BMT Bone marrow failure - prophylactic measure Chemotherapy or irradiation of bone marrow impairing plt production Immune thrombocytopenia -> depending on type Before surgery if low Acute DIC if bleeding Inherited defects Dilutional thrombocytopenia following massive transfusion Auto-immune thrombocyoptenia - depend on type and if bleeding
33
Why do you need to be careful when issuing platelets in a thrombocytopenia
Should first establish cause of thrombocytopenia as plts not always indicated and are sometimes even contraindicated Audits in the past suggest the over-prescribing of plts in these scenarios
34
Talk about platelet transfusion for bone marrow failure
Given prophylactically If count of 10x10^9/L then transfusion indicative In BMT we try to always keep count over 10 Seen in chemo or ablation But if bleeding then as indicated
35
Talk about platelet tranfusions for surgery
50 x 10^9 or less will require tranfusion Very hard to get these counts up to 100 so instead we try to maintain 50 But for normal patients cut off is 100
36
Talk about platelets in DIC
Only given if bleeding with severe thrombocytopenia If you give platelets in the coag phase you will be adding fuel to the fire etc
37
What inherited defect required platelet transfusion
Wiskott-Aldrich Syndrome
38
Talk about refractoriness and anticipation of refractoriness
Anticipation of refractoriness in BMT or bleeding patients Refractoriness is seen in a majority of these patients It is more of a guide for when you should investigate HLA antibodies
39
When are platelets not indicated
HIT Chronic DIC
40
What is refractoriness?
Repeated failure to respond satisfactorily to platelet transfusions and is common in multi-transfused patients >50%
41
What are the common causes of refractoriness?
Anti Class I HLA antibodies or anti HPA Platelet consumption e.g. DIC or drugs or sepsis or bleeding Spleen is seen to consume many platelets in inflammation or trauma
42
Define refractoriness
24 hour platelet increment <5 x10^9/L with two or more consecutive transfusions
43
How is platelet refractoriness treated?
Requires the identification of antibodies and selection of a 'matched' donor e.g. through apheresis NB: matched platelets cost double the price, as the donor will have to be asked to come in Were looking at a prophylactic anti-HLA a1 using MABs but havent been successful yet IVIG can reduce the amount of Ig transfer across the placenta -> occupies binding sites in placenta for Abs to cross-over IUT with compatible platelets Corticosteroids
44
What is NAITP?
Neonatal alloimmune thrombocytopoenic Purpura (NAITP) Platelet equivalent of HDFN
45
How frequent is NAITP
1 in 1500 pregnancies are affected 50% occur in the first pregnancy Usually a sister or a mother will have produced the same antibodies during pregnancy Same frequency as HDFN really Otherwise theres no way of knowing until baby is born with lots of bruising
46
What are the common causes of NAITP?
HPA-1a most common HPA-5b second most common -> platelet antigens are expressed at about 16 weeks -> Ab transferred across placenta at 14 weeks
47
Talk about severity of NAITP
Babies born with bruising Cerebral haemorrhage most severe outcome Severity based on affinity of IgG
48
Clinical features of NAITP
Purpura/bleeding Haemorrhage Hydrocephalus Severity associated with plt count <20 x 10^9/L
49
What HLA is associated with increased severity of NAITP?
HLA-DRB3*0101 allele These are 140 times more likely to make anti-HPA-1a
50
Talk about Post Transfusion Purpura
1:500,000 risk, very rare condition Anamnestic response occuring approximately 1 week post-transfusion Mostly caused by anti-HPA-1a but can cross react with patients own platelets produce an ab against transfused platelets which then react against your own Can cause severe bleeds, plt counts <10 x10^9/L with purpura and haemorrhage Abs tend to cross react so plt tx tend to be ineffective unless large doses fiven to overpower antibodies
51
How is Post transfusion purpura treated
Large doses of platelets Intravenous Ig Steroids Plasma exchange to remove Ab
52
What is TTP
TTP is caused by consumption of platelets in thrombotic lesions Platelet transfusions are not indicated here
53
What is ITP?
Consumption of platelets caused by auto-Abs with broad specificities Chronic vs acute
54
Talk about drug induced thrombocytopenia
Immune complexes bind to platelets which undergo RE removal a la drug induced haemolytic anaemia Transfuse with platelets only in case of major haemorrhage
55
What is heparin induced thrombocytopoenia?
Thrombocytopenia caused by antibodies to heparin-platelet factor 4 complexes These complexes bind to these platelet receptors resulting in activation Thus thrombotic complications Dont give these platelets as they will become activated
56
What is chronic ITP
Seen in adults Insidious onset X2 risk in women Associated with HIV, malignancy and other auto-immune conditions Treated with IVIG, steroids and splenectomy (same as AIHA)
57
What is acute ITP
Usually in children post viral infection Steroids not used in children If older then 6months splenectomy
58
What is DITP?
Drug induced Thrombocytopenia Caused by drugs such as quinine (malaria), sulpha drugs, colloid gold (RA and Alzheimers) Type I = non immune - self resolves Type II = immune, serious, leads to thrombi in 30% of HIT cases and 0.9% of heparin patients
59
How is DITP treated?
Low molecular weight Heparin should be used Or alternatively hirudin (from snake venom) an anti-thrombin drug
60
Risks and Hazards of plts
Febrile and allergic reactions Overload -> as usually given in a major bleed Disease transmission particularly bacteria - staph, strep, serattia Transfusion of rbc alloantibodies Sensitisation to rbc antigens TAGVHD Possible alternative in thrombopoietin TRALI -> not a thing anymore since using male only donors PTP, ABO incompatibliity etc
61
Why is platelet refractoriness often an annoyance?
Plts are often the last thing to increase but you cannot send a patient home with low plts
62
Talk about pathogen inactivation in platelets
We dont do this in ireland but we BacT all of ours Psoralens show promise e.g. S59 Amotosalen-intercept technology is most common
63
Comment on the need for pathogen inactivation of platelets
Frequency as high as 1 in 1,000 Ranges from mild fever to septicaemia to death
64
Talk about psoralens
S59 A group of planar compounds Form adducts with DNA and RNA and when exposed to UV light binding is irreversible, blocking nucleic acid replication Virucidal and bactericidal properties
65
Talk about thrombopoietin
Produced primarily in the liver Considerable homology to EPO Increases with low plts, stimulates plt production by acting on pluripotent stem cells Two main recombinant products available: rTPO and rMGDF
66
Why were TPOs taken off the market
Due to thrombosis formation -> same as EPO
67
Give some other examples of platelet products
Frozen platelets in DMSO Cold stored platelets @4 degrees for up to 2 weeks - being used in the USA in trauma settings - 7 day platelet incubation then 7 days warm - would prevent bacterial growth Anti-fibrinolytic agents such as aprotinin and tranexamic acid DDAVP Lyophilised or freeze-dried platelets - blended into a powder but still seem to work Microspheres of human albumin coated with fibrinogen Thermbospheres - artificial platelets - much easier than red cells to make artifically - due to problems with Hb

4.2 Blood Transfusion Science (21 decks)

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