Blood Bank Basics

Front 1

How much will one unit RBCs raise the hgb & hct?

Back 1

Hgb: 1 g/dl

Hct: 3%

Front 2

How much will one unit plts raise the count?

Back 2

30-60,000

Front 3

What are the indications for washing / leukocyte reduction?

Back 3

1. Risk CMV viremia
2. Decreased formation HLA antibodies
3. Pts with recurrent FNHTR

Front 4

Should platelets be ABO and Rh matched?

Back 4

Yes.

ABO is on platelets (but low density... usu ok if "plasma compatible")
Rh is NOT on platelets but there are some residual RBCs

Front 5

Universal donor?

Back 5

RBCs: O

Front 6

Components of cryo?

Back 6

vWF, factor VIII, factor XIII, fibronectin, fibrinogen

Front 7

Components of FFP?

Back 7

Factor 2,5,10,11... and all factors

Front 8

Uses of FFP

Back 8

Liver disease
Coagulopathy
Warfarin reversal
Vit K def (PT:PTT > 1.5x nl)

Front 9

Uses of cryo

Back 9

DIC (only product with fibrinogen, f'gen<100)
vWF deficiency
factor 13 deficiency

can be used in hemophilia A (some factor 8) but not first line

HAS ABO ANTIBODIES

Front 10

How old do you have to be to donate blood?

Back 10

16

Front 11

Minimum hgb & hct for blood donation

Back 11

12.5 & 38%

11 & 33% for autologous

Front 12

Temperature, pulse, and bp requirements for donation?

Back 12

Max temp 37.5

HR 50-100

bp < 180/100

Front 13

How much whole blood should be drawn?

Back 13

450 +/- 45 mL

Front 14

Storage requirements after donation?

Back 14

1-6C if used for RBCs

20-24C if making other components first; must be stored at 1-6C within 8h for RBCs

Front 15

Common donor reactions?

Back 15

Vasovagal: SLOW heart rate, syncope, nausea. Elevate feet.

Hypovolemia: FAST heart rate, " ". IV fluids.

Hyperventilation

Citrate effect (apheresis donors only): causes hypocalcemia - perioral tingling, arrhythmia, seizure. Slow infusion rate; oral Ca++

Front 16

What are the reasons for indefinite deferral from donating?

Back 16

- Viral hepatitis after age 11
- Parenteral drug use
- Family hx CJD
- Receipt of human dura or pituitary growth hormone
- (+) HbsAG or anti-HBc
- HCV
- HTLV-1
- Travelers to CJD areas
- Use of bovine insulin from UK
- Hx of babesia or Chagas
- Drug: Etretinate
- Receiving money for drugs or sex

Front 17

What testing is required for donor blood?

Back 17

ABO & Rh: Forward AND reverse typing of ABO. Rh type determined by anti-D (forward typing); if -, must test for weak D. Rh- when BOTH are negative.

Antibody screen: in donors with h/o pregnancy or transfusion

Infxs dz: HbsAg, anti-HBc, anti-HCV, HCV RNA, anti-HTLV-1&2, anti-HIV-1&2& HIV RNA, RPR (syphilis), WNV

Front 18

If a patient has been pregnant or transfused in the past 3 months, how close to the date of transfusion must a sample be drawn for testing?

Back 18

Within 3 days

Serum or plasma acceptable

Front 19

How long must a sample be kept after transfusion?

Back 19

7 days

Front 20

What are the common "nuisance" alloantibodies?

Back 20

anti-M, N, Lewis, I, P.

usually detected at room temperature (many labs omit this step and only test at 37C)

Front 21

Pt is A+. What is FORWARD type & REVERSE type?

Back 21

Anti-A: ++
Anti-B: -
Anti-Rh: ++

A cells: -
B cells: ++

(Forward: add antisera to pt blood.
Reverse: add pt's sera to reagent RBCs)

Front 22

What are the 3 columns we use for antibody screening?

Back 22

IS: immediate spin (usu nuisance antibodies; usu IgM)

37C: IgG clinically significant antibodies are warm-acting. Not that useful by itself.

AHG: REQUIRED. antihuman globulin phase, aka "Coombs phase". anti-IgG is added to tube. Detects clinically significant abs.

All should be negative;if (+) perform complete panel.

(Rows are test cells with all impt antigens represented. All group O)

Front 23

What alloantibody is notorious for becoming undetectable over time yet remaining clinically significant?

Back 23

KIDD! (Jka & Jkb)

Front 24

What is dosage effect and which antigens express it?

Back 24

Dosage effect: When an antibody reacts more strongly to homozygous cells than to heterozygous.

Seen in all Rh antibodies EXCEPT D

Classically seen in Kidd, Duffy, Rh, MNS
(Jka, Jkb, Fya, Fyb, DCEce, MNSs)
(basically - seen in all except Lutheran, P, lewis, & Kell)

Front 25

Do we crossmatch blood for infants?

Back 25

Not under 4 months old, unless clinically significant antibodies are detected (may use mom's serum)

Front 26

What is the purpose of crossmatching?

Back 26

Final check on issued blood

Aimed at detecting ABO incompatibility

Performed at room temp ("immediate spin crossmatch); if clinically significant alloantibodies present - must do AHG phase.

Front 27

What are the carbohydrate antigens?

Back 27

ABO, Le, I, M, N, P

Naturally occurring antibodies (usu IgM; rx at room temp; agglutinating)

Front 28

What are the protein antigens?

Back 28

All others!

Antibodies made only after exposure to products with an antigen (usu IgG; rx at 37C; "coating")

Front 29

Describe the ABO antigens

Back 29

Carbohydrates

Genes encode for enzymes (glycosyltransferases) that trx saccharides onto H antigen base

A&B genes on Chrom9 (O allele does not code fxnl enzyme; type 2 H chains fucosylated to H antigen)

Front 30

How is A antigen different from B?

Back 30

A: N-acetyl-galactosamine

B: D-galactose

Front 31

What is the Bombay phenotype?

Back 31

When h gene inherited instead of H. NO H SUBSTANCE PRODUCED.

Extremely rare

Produce dangerous anti-H

Front 32

Which blood groups have more H?

Back 32

O>>A2>B>A2B>A1>A1B

Front 33

What antibodies are present in blood group O?

Back 33

anti-A & anti-B

IgM & IgG

Front 34

What types of blood group A are there?

Back 34

A1 & A2.

A1 cells have more A than A2 cells. 80% are A1; 20% A2.

anti-A1 can be found in up to 5% ppl with A2, 35% A2B

Front 35

What is the most common ABO blood type in whites? blacks?

Back 35

O (~50% each)
A (40%W, 25%B)
B (10%; 20%)
AB (5% each)

Front 36

Rh nomenclature

Back 36

R1: DCe: 40%w, 15%b
R2: DcE: 10% ea
R0: Dce: 5%w, 45%b***
Rz: DCE: rare

r' : dCe: 3% ea
r'' : dcE: rare
r : dce: 40%w, 30%b
ry : dCE: rare

**note these are GENOTYPES. need 2 of the alleles.

Front 37

Most common Rh- & Rh+ genotypes in wh & bl?

Back 37

Rh+ : R1/R1 (DCe) or R1/r (DCE/dce) in wh

R0/R0 (Dce/Dce) or R0/r (Dce/dce) in blacks

Rh-: r/r (dce/dce) in BOTH

** R0 most common allele in bl (rare in wh)

Rh- : r/r (dce/dce)

Front 38

How does a weak D react with anti-D reagent?

Back 38

negative in IS
negative at 37C
POSITIVE at AHG phase

Front 39

What causes weak D phenotype?

Back 39

Quantitative WEAK D: most common. gene alteration, reduced D antigen expression
(common in bl - Dce haplotype (R0) - due to position of C)

PARTIAL D: RBCs lack epitope(s) of D antigen.
**partial-D women at risk of forming anti-D to D+ fetus

Front 40

Does transfusion of weak D into D- pt result in immune response?

Back 40

Only if pt previously sensitized

Front 41

Do we test & label for weak D?

Back 41

We test DONOR samples for weak D

Labeled D+ if present

Recipient not tested

Front 42

What is Rh null?

Back 42

No Rh antigens
(no Rh or RhAG (Rh assoc glycoprotein)

** Lack LW, Fy5. Weakened S, s, U

** Structural abnormalities (stomatocytosis!)

Front 43

What is the most immunogenic antigen that is non-ABO?

Back 43

D!

80% D- pts will develop anti-D after exposure to a single unit

Front 44

What units should be selected for a patient with anti-E?

Back 44

E-negative, c-negative

This is because most ppl with antiE are R1/R1 (DCe/DCe) and have been transfused with R2 blood (DcE), thus acquiring an anti-E and anti-c. Anti-c is often too weak to detect but is a COMMON CAUSE OF DHTR.

Front 45

RBCs are negatively charged... How can we get them closer together to speed up testing?

Back 45

Add a potentiator to the antibody screen at 37 & AHG phases

LISS, PEG, bovine albumin

Front 46

When is adding anti-C3d helpful in the AHG phase of antibody screening? (as opposed to anti-IgG that is normally used)

Back 46

- C3d is a nonreactive byproduct of complement fixation on RBCs
- Anti-C3d is useful for evaluating IgM-related hemolysis and cold agglutinin disease, where antibodies are not usually detectable via anti-IgG

Front 47

How are proteolytic enzymes used in pretransfusion testing, and what antigens do they affect?

Back 47

Cleave proteins on RBC surface, may make underlying antigens more available

Destroys some antigens (e.g., Duffy and MNS), enhances others (ABO, Rh, Jk)

Front 48

What is adsorption?

Back 48

Removal of specific antibodies from sample via incubation with antigen-positive RBCs

Used to remove warm or cold autoantibodies (“autoadsorption”) from sample in order to detect underlying alloantibodies

May also be used to remove one or more alloantibodies (“alloadsorption”) from sample in order to detect or confirm the presence of other alloantibodies

e.g., Sample has anti-K, anti-C, and anti-S but anti-S isn’t visualized well. Use K+C+S– RBCs to adsorb the anti-K and anti-C and leave the anti-S in the “adsorbed serum” for clearer results

Front 49

What is elution?

Back 49

Technique for removal of antibodies bound to RBC surface for analysis.
May be done with heat, cold, chemical (e.g., glycine) treatment

Front 50

How is DTT/2ME used in pretransfusion testing?

Chloroquine?

Back 50

Dithiothreitol (DTT) or 2-mercaptoethanol (2-ME) denatures surface RBC antigens of multiple groups (including Kell, Lutheran, Dombrock, Yt, LW). Can also be used to remove IgM antibody activity from serum

Chloroquine removes IgG from coated (DAT-positive) RBCs to allow for accurate phenotyping (effective at least 80% of the time). Also removes residual HLA antigens from RBCs