Immunohematology Flashcards

1
Q

What does the H-gene code for?

A

L-fucose which binds to RBC oligosaccharide side chains

(person may be HH or Hh and still produce the enzyme (L-fucosyltransferase), but hh produces no enzyme))

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2
Q

A gene adds ____ to L-fucose; B gene adds _____ to L-fucose.

A
  • N-acetylgalactosamine
  • D-galactose

(O gene→ oligosaccharide chain + L-fucose)

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3
Q

Bombay blood type

A

homozygous hh → no pre-cursor antigen H (L-fucose) → no A or B expression

(L-fucose allows expression of A and/or B Ags on RBC)

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4
Q

Bombay Blood group appears to be ____ type blood.

A

O type

(serum from Bombay individual will agglutinate type O cells; they have anti-A, anti-B, anti-H Abs)

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5
Q

Landsteiner’s Law

A

When sugar antigen is present on the RBC, the corresponding Ab will be absent from the serum

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6
Q

Blood antigens are not consistent; give 3 examples of blood antigens that change over time

A
  1. I Antigen: ⇡ w/maturity
  2. Lewis group: ⇣ in pregnancy
  3. A/B Ags: altered w/disease
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7
Q

Non-immune antibody

A

IgM: anti-A & anti-B (made w/o previous exposure)

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8
Q

IgM & IgG can both fix complement, but IgG must _____

A

have another IgG to do it; IgM only needs one

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9
Q

Forward typing tests for _____; Reverse typing tests for _____.

A
  • blood group Ag (on RBCs)
  • serum Ab

(must match them, forward typing = blood group Ag testing)

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10
Q

What does a positive Direct Coomb’s Test indicated?

A

patient serum has IgG Abs bound to the RBCs

(ex: erythroblastosis fetalis)

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11
Q

What does a positive Indirect Coomb’s Test indicate?

A

serum Ab

(ex: Rh- mother gets tested to see if she has anti-RhD abs that will attack an Rh+ fetus)

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12
Q

What is the difference between warm & cold agglutinins?

A
  • warm: IgG, reacts at body temp (35-37 C) → cause immune response
  • cold: IgM, react at temps below body temp (Ii system)

(both are Abs against blood group Ags. Warm = clinically relevant)

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13
Q

Warm agglutinins can cause ______.

A

hemolytic transfusion reactions

(prior exposure → ab production (warm agglutinin))

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14
Q

Agglutination is a _____ reaction

A

serologic

(RBCs Ag forms parrticles when coated in Abs)

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15
Q

In In vitro agglutination reactions, IgG are _______(always/not at all) visible w/RBC ags; IgM are _______ (always/not at all) visible

A
  • not at all
  • always

(IgGs are small and RBC are usually far apart)

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16
Q

Hemolysis

A

Ab-coating → complement activation = lysis

(pink-red supernatant from freed Hgb. This cannot be used for lab testing!)

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17
Q

Blood transfusion is a transplanted tissue aka, ______. The blood component is only need for a limited amount of time because _____.

A
  • liquid allograft
  • the patient’s bone marrow make up the loss

(blood does NOT have MHC I/II → safer to transplant than other tissue)

18
Q

In the ABO system, structural polymorphism is the _____.

A

carbohydrate component of glycolipid/glycoprotein (band 3) on RBC membrane

19
Q

A & B antigens (on RBCs) have structural similarities to ________.

A

commensal bacteria

(that is how they are made w/o exposure)

20
Q

Hemolytic disease of the newborn is caused by _______.

A

RhD- mother has RhD+ baby → at birth, mom is sensitizes to RhD+ → antibodies will attack future RhD+ baby → hemolytic disease of the 2nd baby

21
Q

hemolytic reaction is a _______ reaction to the _____.

A
  • type II hypersensitivity
  • Ag on RBC/additional sugar on cell-surface glycolipids
22
Q

What is a cross-match test?

A

patients serum is tested before transfusion against ABO/RhD matched donors; only RBC NOT BOUND by Abs may be used otherwise → hemolytic reaction

(donor serum not tested w/patient RBC bc there isn’t enough Ab to show agglutination rxn)

23
Q

AHG

A

anti-human globulin (IgG)

23
Q

Genotype AA, AO = _____ phenotype

Genotype BB, BO = ______ phenotype

A
  • Type A blood Ag
  • Type B blood Ag
24
Q

Genotype AB = _____ phenotype

A

Type AB blood Ag

25
Q

A “secretor” is a person who secretes ______.

A

their blood type Ag into body fluids & secretions

(ex: saliva)

26
Q

D antigen aka _____

A

Rh factor

27
Q

D mosaic

A

patient has inherited some Rh+ antigen

27
Q

Weak expression of D

A

partial Rh+ that does not react w/Anti-D antibodies (anti-Rh)

28
Q

Weak D expression causes (3)

A
  1. Genetic: low density of D Ag
  2. Position: trans position of C gene → D gene
  3. Mosaic: partial D expression (absence of portion of D Ag)
29
Q

Lack of Duffy antigens is associated with ______.

A

resistance to malaria

30
Q

The Kidd System has 3 alleles, which are codominant?

A
  • Jka
  • Jkb
31
Q

Rhnull results in ______

A

hemolytic anemia (membrane is defective→osmotic fragility)

32
Q

Symptoms of Rhnull

A
  1. hemolysis
  2. stomatocystosis
  3. spherocytosis
  4. osmotic fragility

(they may only receive blood from other Rhnull)

33
Q

P System

A

Patients have an anti-P antibody → fixes complement & on RBCs that are in the peripheral extremities (reduced temperature) → hemolysis when blood is warmed

(cold paroxysmal hemoglobinuria (PCH)/autoimmune hemolytic anemia)

34
Q

P system is aka _____

A

Donath-Landsteiner antibody

35
Q

Why is Ii system considered a nuisance?

A

Cold agglutinins encountered during lab testing & hides clinically significant antibodies which react at body temperature or with AHG

36
Q

In the Kell system, there are 21 antigens. What is the clinical relevance of the Kell System?

A
  • Anti-K (IgG) antibodies are the 2nd most antigenic ab
  • associated w/HDN & transfusion reactions

(compatible blood is difficult to find for this blood group)

37
Q

Kernicterus aka bilirubin encephalopathy is caused by _____

A

bilirubin deposits in the brain cells (>25 mg/dL)

38
Q

What is RhoGAM?

A

Rho Immune globulin → binds to fetal RBC & removes them → mother does not make Anti-Rh Ab

(given at 30 weeks, and again 3 days after birth if baby is Rh+)