Blood groups and blood transfusions Flashcards

1
Q

ABO typing

A
  • Karl Landsteiner discovered if he added red cells and plasma of 6 different colleagues the samples would agglutinate
  • ABO system is so potently antigenic because the corresponding antibodies to each antigen occur naturally
  • ABO antigens are inherited in a mendelian pattern – each group has 25% chance of production, genes code for its enzyme rather than for the sugar itself
  • Another gene also codes for the sugar base the ‘A’ or ‘B’
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2
Q

ABO antibodies development

A
  • Theories they develop against environmental antigens
  • Infants <3 months will produce little to no antibodies (maternal prior to this)
  • First true antibodies will be >3 months
  • Maximal titre 5-10 years
  • Titre decreases as we age
  • Mixture of IgM and IgG
  • IgM mainly for group A and B
  • Wide thermal range means they are able to react at 37
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3
Q

Rhesus antigens

A
  • Over 45 different antigens
  • Genetic locus on chromosome 1 (co-dominant allele, 2 genes, RHD (coding for Rh D), RHCE (coding for Rh C and Rh E))
  • Highly immunogenic – high proportion of D neg people will form anti-D if exposed to D pos blood
  • Can cause haemolytic transfusion reactions and haemolytic disease of the fetus and newborn (HDFN)
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4
Q

HDFN

A
  • Haemolytic disease of the fetus/newborn
  • Rh D sensation most common cause (but there are others)
  • Development of antibodies from sensitising event – severe fetal aneamia
  • Hydrops fetalis
  • Prevention: detect mothers risk, maternal fetal free DNA, anti D prophylaxis
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5
Q

cross-matching blood

A
  • Units of blood deemed to be suitable will be chosen from the stocks available
  • Either an exact match (eg. A+ for A+)
  • Or ‘compatible’ blood (eg. O- for A+)
  • Serological test
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6
Q

Direct Antiglobulin Test (DAT or direct coombs test)

A
  • Blood grouping for ABO and rhesus D = indirect antiglobulin test – detecting Ab in patients serum
  • Method needed to detect Ab already on RBCs
  • Indicated – patients with possible autoimmune haemolysis, transfusion reactions, detecting haemolysis due to fetal/maternal group incompatibility, can be positive for many other reasons too unfortunately (many of which are clinically significant)
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7
Q

donation

A

Donation: donors screened, questionnaire, body weight (min 50kg), test for anaemia, temporary and permanent exclusion, either whole blood or apheresis – blood is removed and separated externally and then the components not needed are returned
Tests on donations: mandatory – Hep B, HIV, Hep C, Syphilis, Human T cell lymphotropic virus, groups and antibodies : some are tested for CMV, malaria, west nile virus, typanosoma

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8
Q

separation and storage

A
  • Whole blood donated into closed system bags
  • Blood spun to separate down to packed red cells/ buffy coat and plasma
  • Plasma only kept from male donors
  • Plasma can be frozen to make FFP (or further processed to make cryoprecipitate)
  • Red cells kept at ambient temperature for a short time then passed through a leucodepletion filter and resuspended in additive
  • Buffy coats pooled with donations of matching ABO and D type and then leucodepleted to make platelets
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9
Q

blood products

A
  • Stored at 4◦C, shelf life of 35 days
  • Some units will be irradiated (to eliminate risk of transfusion associated graft vs host disease
  • Indications: severe anaemia (not purely iron deficiency)
  • Transfusion threshold: <70 or <80 if symptomatic, transfuse 1 unit and re-check (unless massive transfusion required)
  • Emergency stocks of O Rh D-blood available in certain areas in the hospital (A+E, maternity)
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10
Q

platelets

A
  • Most units are pooled from 4 donations
  • Some single donor apheresis units
  • Stored at 22◦C with continuous agitation
  • 7 day shelf life if they are monitored for bacterial contamination
  • Indications: Thrombocytopenia and bleeding, severe thrombocytopenia <10 due to marrow failure
  • ABO type still important (antibodies present in plasma still able to cause recipient red cell haemolysis)
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11
Q

fresh frozen plasma

A
  • From whole blood donations or apheresis
  • From male donors only
  • Patients born >1996 , can only receive plasma from low vCID risk (not UK plasma)
  • Single donor packs have variable amounts of clotting factor, Pooled versions can be more standardized
  • Indications: multiple clotting factor deficiencies and bleeding (DIC), come single clotting factor deficiencies where a concentrate isn’t available
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12
Q

Cryoprecipitate

A
  • Made by thawing FFP to 4◦C and skimming off fibrinogen rich layer
  • Therapeutic dose is 2 packs each pooled from 5 donations of plasma
  • Used in DIC with bleeding and massive transfusion
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13
Q

Immunoglobulin (IVIg)

A
  • Made from large pools of donor plasma
  • Normal IVIg: contains Ab to viruses common in the population, used predominantly in immune conditions such as ITP
  • Specific IVIg: from selected patients, known high Ab levels to particular infections/ conditions ( anti D immunoglobulin used in pregnancy, VZV immunoglobulin in severe infection)
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14
Q

Granulocytes

A
  • Used very rarely
  • Effectiveness controversial
  • For severely neutropenic patients with life threatening bacterial infections
  • Must be irradiated
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15
Q

Factor concentrates

A

Single factor concentrates:
• Factor VIII for severe haemophilia A (recombinant version which carries no risk of viral or prion transmission)
• Fibrinogen concentrate (factor I)
Prothrombin complex concentrate (Beriplex, Octaplex)
• Multiple factors
• Rapid reversal of warfarin

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16
Q

safe delivery of blood

A
  • Patient identification
  • 2 sample rule
  • Hand-written patient details
  • Blood selected and serologically cross matched
  • Mistakes can still happen – most common patient identification errors, wrong blood in the wrong tube, laboratory errors
  • Blood transfusions delayed
  • Too much blood transfused
17
Q

avoidance of transfusion

A
  • Optimise patients with planned surgical procedures pre-op
  • Use of erythropoietin stimulating drugs – particularly useful in renal failure, licensed for patients with cancers too
  • Intra-operatively – cell savage
  • IV iron for severe iron deficiency
  • Some patients may tolerate lower Hbs and if well, not required transfusions at all – sickle cell disease
18
Q

Haemolytic reaction

A
  • Most serious ABO incompatibility: rapid intravascular haemolysis, cytokine release, acute renal failure and shock, dissemination intravascular coagulation, can be rapidly fatal
  • Treatment: stop the transfusion immediately, fluid resuscitate – A, B, C
  • Can be acute or delayed (delayed = >24 hours after transfusion)
  • Need to be reported to SHORT (serious hazards of transfusion)
19
Q

bacterial contamination

A
  • More often with platelets (still very rare)
  • Occurs very soon after transfusion started
  • Typical symptoms: fevers, hypotension, shock
  • Inspection of the unit may show abnormal colouration/ cloudiness
20
Q

TRALI (transfusion-related lung injury)

A
  • Caused by Ab in donor blood reacting with recipient pulmonary endothelium/ neutrophils
  • Inflammatory cells cause plasma to leak into alveolar spaces
  • Symptoms: SOB, cough production of frothy sputum, hypotension, fever
  • Treatment – supportive
21
Q

TACI (transfusion-associated circulatory overload)

A
  • Acute or worsening pulmonary oedema within 6 hours of transfusion
  • One of the most common adverse events related to transfusion
  • Older patients at more risk
  • Symptoms: respiratory distress, evidence of positive fluid balance, raised blood pressure
  • Careful assessment of transfusion need and limiting amount can help to avoid