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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
Q

How are platelets stored

A

@22 degrees

Maintained pH of 6 or above

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26
Q

What is the ratio of PAS to palsma in pooled units

A

75% PAS and 25% plasma

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27
Q

What donors do we use for plasma and why?

A

Male only
No HLA antibodies
Avoid Trali

28
Q

Since when have we been irradiating platelets and why?

A

Since 1998

Reduce FNHTR

Reduce refractoriness

29
Q

Talk about apheresis donation

A

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
Q

What are some alternatives to PAS

A

Electrolyte solutions containing acetate, citrate, phosphate and chloride

31
Q

For how long are platelets stored and in what

A

Constant controlled agitation with gaseous exchange

Polyolefin packs

7 day storage (used to be 5 days)

32
Q

When are platelets indicated?

A

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
Q

Why do you need to be careful when issuing platelets in a thrombocytopenia

A

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
Q

Talk about platelet transfusion for bone marrow failure

A

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
Q

Talk about platelet tranfusions for surgery

A

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
Q

Talk about platelets in DIC

A

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
Q

What inherited defect required platelet transfusion

A

Wiskott-Aldrich Syndrome

38
Q

Talk about refractoriness and anticipation of refractoriness

A

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
Q

When are platelets not indicated

A

HIT

Chronic DIC

40
Q

What is refractoriness?

A

Repeated failure to respond satisfactorily to platelet transfusions and is common in multi-transfused patients >50%

41
Q

What are the common causes of refractoriness?

A

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
Q

Define refractoriness

A

24 hour platelet increment <5 x10^9/L with two or more consecutive transfusions

43
Q

How is platelet refractoriness treated?

A

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
Q

What is NAITP?

A

Neonatal alloimmune thrombocytopoenic Purpura (NAITP)

Platelet equivalent of HDFN

45
Q

How frequent is NAITP

A

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
Q

What are the common causes of NAITP?

A

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
Q

Talk about severity of NAITP

A

Babies born with bruising

Cerebral haemorrhage most severe outcome

Severity based on affinity of IgG

48
Q

Clinical features of NAITP

A

Purpura/bleeding
Haemorrhage
Hydrocephalus
Severity associated with plt count <20 x 10^9/L

49
Q

What HLA is associated with increased severity of NAITP?

A

HLA-DRB3*0101 allele

These are 140 times more likely to make anti-HPA-1a

50
Q

Talk about Post Transfusion Purpura

A

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
Q

How is Post transfusion purpura treated

A

Large doses of platelets

Intravenous Ig

Steroids

Plasma exchange to remove Ab

52
Q

What is TTP

A

TTP is caused by consumption of platelets in thrombotic lesions

Platelet transfusions are not indicated here

53
Q

What is ITP?

A

Consumption of platelets caused by auto-Abs with broad specificities

Chronic vs acute

54
Q

Talk about drug induced thrombocytopenia

A

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
Q

What is heparin induced thrombocytopoenia?

A

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
Q

What is chronic ITP

A

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
Q

What is acute ITP

A

Usually in children post viral infection

Steroids not used in children

If older then 6months splenectomy

58
Q

What is DITP?

A

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
Q

How is DITP treated?

A

Low molecular weight Heparin should be used

Or alternatively hirudin (from snake venom) an anti-thrombin drug

60
Q

Risks and Hazards of plts

A

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
Q

Why is platelet refractoriness often an annoyance?

A

Plts are often the last thing to increase but you cannot send a patient home with low plts

62
Q

Talk about pathogen inactivation in platelets

A

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
Q

Comment on the need for pathogen inactivation of platelets

A

Frequency as high as 1 in 1,000

Ranges from mild fever to septicaemia to death

64
Q

Talk about psoralens

A

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
Q

Talk about thrombopoietin

A

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
Q

Why were TPOs taken off the market

A

Due to thrombosis formation
-> same as EPO

67
Q

Give some other examples of platelet products

A

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 (13 decks)

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