Blood Bank from Osler Flashcards Preview

Blood Bank/Transufsions > Blood Bank from Osler > Flashcards

Flashcards in Blood Bank from Osler Deck (53)
Loading flashcards...

Stronger agglutination IgM vs IgG?


Extravascular hemolysis raises what lab?


What are the two Antiglobulin reagents used?

IgM agglutinates more (Pentamere)




Anti-IgG and C3d: polyspecific

Anti-IgG and be poly or mono


If no agglutination what must be done?

Check cells; RBCs with IgG attached to them 


Which ABO groups Enhance with enzymes?



"A Rotten Kid": ABO/H, Lewis, I, P, Rh, Kidd


Decreased: "My Dog Lassie" MNS, Duffy, Lutheran


Unaffected? Kell, Diego, Colton


Anti-P1 neutralized by?

Anti lewis?

Anti-Chadio and Rodgers?


P1; Hydadid cyst fluid, prigeon dropping, turtledoves egg white

Lewis: Plasma or serum, saliva

Chadio/Rogers: Serum (complement)

Sd: Urine

I: Human breast milk


What lechtin binds A1?


O and H?



T, Tn?


A: Dolichous biflorurus
B: Banderiraea simplicifolia

O: Ulex europaeus

N: Vicea gramlnea

T: Arachis hypogea

T/Tn: Glycine Max

Tn: Salvia


ABO Chr, Rh?


Warm antibodies are IgG or M and do they cause HDFN or HTR?

ABO 9; Rh 1


IgG and do cause HDFN and HTR

Cold tends to be IgM and "natural" BUT EXCEPTION IS ABO!!!


Type 1 or 2 most common on red cells?

Type 1 chain has what type of linkage, seen in?

Type 2 linkage, seen in?

What gene adds FUT to type 2 to make H; Type 1?

Type 2

Type 1; Beta 1-3 linkage; Gal to GalNAc; seen in secreations glycoprotein/glycoplipids

Type 2: Beta 1-4 Gal-GalNAc; RBC membrames and glycolipids

FUT1 added to type 2 makes H antigen (RED CELLS); FUT2 adds Fuctose to Type 1 (SECRETING CELLS)

FUT1 found on ~100% of people and FUT2 in 80% of people


Blood group A has fuctuose on what sugar?


Which group has the most H?

Least H?

A: GalNAc conntect to Gal with Fructose
B: Gal to Gal with Fructose

Most: O (Auto recessive), Least: AB


Do ABO antibodies deacrease during life?


Which Anti-A, B, AB antiboies are IgG, why do we care?


Most common blood types?

Yes; drops in elderly 


Anti-A, and Anti-B, Not anti-A,B; CROSS PLACENTA




Percent of group A1 and A2?

Why do we care?

What lectin can be used to detect this?

80% A1; 20% A2

Anti-A1 at 37 degrees can cause reaction to A blood

Dolichos biflorus detects A1 but not A2


Reasons that Forward cell grouping does not equal serum grouping?

ABO Subgroups



Acquired B (AB patient with bacterial infection)


What is acquired B?

Associated with?

Forward and reverse type?

A1 RBCs contact enteric gram negative organisms; End GalNAC deacytylated to Gal-amine similar to B 

AW: Colon cancer, GI obstruction, gram - sepsis

Forward: AB (strong A and weaker B), Reverse A


What phenotype lacks H?

What gene is missing?

Forward and reverse screen?
What is Para-Bombay?

Both need?

Bombay (Oh); NO H, A or B

Lacks FUT1 (H) and FUT2 (Secretor)
Forward O, Reverse: O; Screen: POSITIVE


Para-Bombay: Ah, Bh, ABh, Nonfunctional FUT1, at least one Functional FUT2, may have Anti-H

H negative blood


What gene makes the Lewis?

What makes the Lewis system different from other Blood groups?

Is it clinically significant, what type of antibody?

Neutralized by?

Who tends to lack Lewis antibodies?

FUT3 makes lewis (Lewis A; not secreted); FUT2 secretor can make lewis b (secreted)

Lewis is Adsorbed; LeB is better than A; Adults normally Le(a neg, b positive)

Not really significant, IgM

Secretor saliva



H. Pylori and Norwalk virus attach to what antigens?

Le A and B negative kids susceptibilitiy increased to?

H and Le b


E. Coli and UTIs


I system has what type of chains?
Who is I and i seen in?


Auto-I seen in?
Auto-i seen in?



ABO type 2 chains; related to chain complexity
I: Adults (branced) i: babies (linear)

Big I in big people


Auto-Anti-I: Myoplasma pneuomonia and cold agglutinin

Auto-Anti-i: EBV


What receptor is for Parvo B19?

Why do we care about this group?


What is paroxysmal cold hemoglobinuria association?

How to collect tubes?


99% patients are P1+, 1% P2 and have anti-P1 antibody which can cause Acute HTRs and spontaneous abortions


Biphasic IgG hemolysin from Auto Anti-P; Syphilis and viral infection
Collect at 37 degrees C; lyses at room temp


What antigens are in Rh blood group?


Common cause of D negative?

Capital R indicates, little r, and 1 or ' and ''?

D, C, E, c, e; Rh+=D



R/r=D or d

1 or ': C

2 or '': E


What race is more common to be R zero (Dce)?

Who has more R1 (DCe)?

(Dce) seen in Blacks and less common whites

R1 most common in whites (DCe) and least common in blacks


Rh antibodies IgG or M?

What percent of Rh- who get Rh+ make antibody?

Why do we care?

 Warm IgG

20-30% with single unit of RBCs

Severe HDFN, extravascular


What is weak D?

What is partial ?


Weak: D detected at IAT and 37 degree C and not at immeidate spin or 37 degree!


Partial: Lack soem D epitopes; may have Antibodies to missing parts: Might need molecular testing; test as Rh positive but give Rh+ blood and they develop Anti-D


Rules of B's?


What does Kidd antibodies do?

Why do we care about Kidd?

If you have an A antigen and B antigen; the B is more common EXCEPT IN KIDD!


More exposure means more/stronger antibodies!; IgG and IgM that fixes complement?


Reaction/antibody to Kidd can disappear until given blood then HEMOLYTIC REACTION


MNS seen on?

Why do we care?


Glycopherin A (M and N) and B (S, s,, U)

<1% of blacks are S-s-U- so sickle cell patients; Get Anti-S, s, and U which cause hemolysis

Vicea graminesia acts as anti-N


Duffy is negative in what population?

IgG or M antibodies?

Big worry?

Common Duffy NEGATIVE in blacks (so have anti-body) and rare in caucasians; 

Duffy glycoprotein is receptor to P. Vivax; Fy (y close to V mnemonnic)


Delayed HTR


Big K present in and little k?


What is Xk?


Is anti-K common?

What is Kell null (K0)

Big K: 9% white, 2% black  Little k: 99.8%


Xk protein express Kx blood group antigen and closs to K antigens on RBC surface

Anti-K: second most antigenic after anti D; Exposure requring warm IgG, Severe HTR and HDFN

Anti-k: Like anti-K but only 0.2%

K0: Lacks kell antigens an dhas Anti-Ku; needs Kell null individuals


What is Mcleod syndrome, and inheritience?

Caused by?


Why do we care?

X-linked recessive

Acantholytic hemolytic anemia, Chronic granulomatous disease association

Abscense of Kx antigen and decreased Kell antigens


Transfused patients make anti-K and anti-Kx making it impossible to find donors



Blood sugar that defines Blood group A?


A: N-acetyl-D-galactosamine

B: D-galactose

H: L-fucose


Who regulates blood banks?
Who accredits them?

FDA regulated, AABB accredits


Donation dates (from last):
Whole blood?

Infrequent plasmapheresis?
Single apheresis?

Double/Triple apheresis?

Whole blood: > or equal 8 weeks

DRBC: > or equal 16 weeks
Infrequent plasmaphoresis: > or equal 4 week

Single apheresis: > or equal 48 hrs.

Double/Triple: > or equal 7 days


Permanent deferals, viruses?


Graft of what, meds?



HIV (IVDA); Paid for sex/drugs, Human GH pre 1985 (from cadavers), HBV, HCV, HIV, HTLV

DURA MATER GRAFT, BOVINE INSULIN from UK, Teratogens, Etretinate (Tegison)


As of 2017 no longer permanent