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Book - Transfusion Medicine for Pathologists > BBGuy & Notes > Flashcards

BBGuy & Notes Flashcards

1
Q

What is the “sensitization” phase of agglutination, and how do enhancement media facilitate it?

A

Coating of red cells by antibody.
LISS: Decreases zeta-potential, enhances COLD Ab
PEG: Excludes H2O, enhances WARM Ab

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2
Q

What is the “lattice/bridging” phase of agglutination?

A

When antibodies and RBCs crosslink to actually agglutinate. IgM is better at this than IgG due to size.

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3
Q

Describe the process of the IS phase and 37C phase. Include incubations.

A

IS: 1 drop 2-5% RBCs, 2 drops serum, spin 15-30sec.
37C: Same ratio, with 10-15min for LISS, 15-30min for PEG/albumin, 30-60min for no potentiation.

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4
Q

What is the most sensitive system for tube testing?

A

PEG (similar to gel testing)

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5
Q

How are the results of solid-phase red-cell adherence testing interpreted?

A

Indicator RBCs coated with IgG are used to attach to test RBCs. A tight button is negative, a spread “carpet” is positive.

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6
Q

Distinguish between the antiglobulins used in antiglobulin testing.

A

Anti-IgG: Used for PEG, gel, and solid phase tests. Detects IgG-coated red cells.
Anti-C3b/d: Detects complement components, most useful in IgM and cold-agglutinin.

Polyspecific: Both. Usually the first choice.

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7
Q

What is the role of a check cell?

A

A positive control used after a negative DAT/IAT tube test to ensure functioning of AHG reagent.

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8
Q

What blood group systems demonstrate dosage effect?

A

Rh
Duffy
Kidd
MNS

(Kell, but this will rarely be observed)

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9
Q

What blood groups are enhanced by enzyme treatment?

A

ABO-related
Rh
Kidd

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10
Q

What blood groups are diminished by enzyme treatment?

A

Duffy
MNS
Lutheran

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11
Q

What are some sources of neutralizing substances for:

  1. ABO
  2. Lewis
  3. P1
  4. Sda
  5. Chido, Rodgers
A

1, 2. Saliva of secretors

  1. Hydatic cyst fluid, pigeon egg-whites
  2. Human urine
  3. Human serum
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12
Q

Recall 6 lectins and their antigen specificity.

A 
Dolichos biflorus - A1
Ulex europeaus - H
Vicia graminea - N
Arachis hypogea - T
Glycine max - T, Tn
Salvia - Tn
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13
Q

Distinguish between Type 1 and Type 2 chains. What acts on each?

A

Type 1: Free-floating antigens, secreted. Acted upon by FUT2 (Se) to make Type 1H antigen

Type 2: Bound antigens. Acted upon by FUT1 (H) to make Type 2H antigen

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14
Q

How common are the FUT1 and FUT2 genes? What are the consequences of lacking each?

A

FUT1 is ubiquitous; absence results in Bombay phenotype.

FUT2 expressed in 80%; absence results in non-secretor phenotype.

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15
Q

What is the terminal sugar in group A sugars? Group B?

A

A: N-acetylgalactosamine
B: Galactose

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16
Q

Recite the blood groups (incl. subgroups) by level of H expression.

A

O > A2 > B > A2B > A1 > A1B

17
Q

Trace the expression of ABO antigens in gestation and childhood.

A

ABO antigens first appear at 6wks gestation, but don’t reach adult levels until age 4.

18
Q

Trace the expression of ABO antibodies in gestation and childhood.

A

Begin to appear at 4mo age, reach adult levels by age 10, then fall off with advanced age.

19
Q

What are the three types of ABO antibodies?

A

Anti-A or -B IgM expressed by B/A
Anti-A or -B IgG expressed by O
Anti-A,B IgG expressed by O

20
Q

How do ABO group frequencies differ by race?

A

Whites have relatively more A-groups. Blacks and Asians have relatively more B-groups. Native Americans are largely just O-group

21
Q

How often do A2 or A2B patients produce Anti-A1?

A

1-8% of A2 and 25% of A2B will form Anti-A1.

22
Q

What is B(A) phenotype?

A

Group B patients with weak A activity; an inherited condition that looks like the opposite of acquired B.

23
Q

What is the difference between LeA and LeB?

A

LeB is the product made when Se acts before Le(FUT3). It is generally more abundant than LeA in secretors.

24
Q

What is the racial makeup of Lewis antigens?

A

Black patients are more likely to be Le/FUT3 negative than white patients.

25
Q

What are the infectious associations of the Lewis system?

A

H. Pylori and Norwalkvirus attach via Leb antigen. Le(a-b-) patients are at increased risk for Candida and E. Coli infections.

26
Q

What are the I antigens?

A

Built on type 2 chains, expression of big-I increases with age (except in some asians, “i-adult”).

27
Q

What are the classic associations of:

  1. Auto-anti-I
  2. Auto-anti-i
  3. i-adult phenotype
A
  1. Cold agglutinin disease, mycoplasma pneumoniae infection.
  2. Infectious mononucleosis
  3. Cataracts, HEMPAS
28
Q

What diseases are associated with the P-system?

A

P antigen is a parvovirus receptor.
Anti-P antibodies are associated with paroxysmal cold hemoglobinuria (biphasic IgG binds in cold, lyses in warm; “Donath-Landsteiner”)

29
Q

Recall three basic rules of Wiener haplotype prevalence.

A
  1. R1 always comes before R2
  2. r is always #2
  3. R0 is #1 in blacks, #4 in whites
30
Q

What are the big four Wiener haplotypes in whites and blacks?

A

White: R1 > r > R2 > R0
Black: R0 > r > R1 > R2

31
Q

How do different races mechanistically lose the D-antigen?

A

Caucasians: Deletion of RHD gene
Africans: Point mutations of RHD gene (“pseudogene”)
Asians: Inactive RHD gene

32
Q

Summarize weak D phenotype.

A

D is present in very low level, requiring AHG/IAT testing to detect (test negative in IS). To avoid alloimmunizing a D-negative patient, test all donors and D-negative babies in AHG.

33
Q

Summarize partial D phenotype.

A

Various epitopes of D antigen are missing. These patients may type as D but can still form Anti-D. May be hard to detect; try to give partial D mothers RhoGAM.

34
Q

What is “D-E-L”?

A

In a third of D-negative asians, tiny amounts of D can actually still be found (different than weak D, as can only be detected on elution of reagent anti-D?)

35
Q

What is the “G” Rh antigen?

A

An antigen that is present when either C or D are present. Suspect when a D-negative patient forms an anti-D when not obviously exposed to D.

36
Q

What is the “f” Rh antigen?

A

Present when RHce is inherited (r and R0). Anti-f can be seen togther with anti-c or anti-e.

Book - Transfusion Medicine for Pathologists (13 decks)

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