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Immunohematology Lec > OTHER BLOOD GROUP SYSTEMS PART 3 (LU) > Flashcards

OTHER BLOOD GROUP SYSTEMS PART 3 (LU) Flashcards

1
Q

• (?) were first recognized in 1945 when (?) was discovered in a patient with lupus erythematosus diffusus after receiving a transfusion with blood carrying the low-incidence antigen.

A

Lutheran antigens

anti-Lua

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2
Q

was misinterpreted as Lutheran, derived from the donor’s name Luteran

A

• Anti-Lua

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3
Q

Subsequently, [?], the antithetical partner to Lua, was described in 1956.

A

anti-Lub

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4
Q

was described in 1961, demonstrating dominant inheritance, contrary to most null phenotypes at the time.

A

Lu(a-b-)

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5
Q

inherited as a recessive silent allele was identified.

A

Lu(a-b-)

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6
Q

were used to test antibodies to unknown high-incidence antigens.

A

Rare Lu(a-b-) RBCs

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7
Q

Some sera showed a phenotypic relationship to Lutheran, reacting with all RBCs except

A

Lu(a-b-)

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8
Q

These specificities were given numeric designations (?) to represent their association with the Lutheran system.

A

Lu4, Lu5, Lub, etc.

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9
Q

Three pairs of antithetical antigens (?) have been shown to be inherited at the Lutheran locus.

A

Lu6 and Lu9, Lu8 and Lu14, Lu18 and Lu19

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10
Q

Several antigens have been shown to be located on the Lutheran glycoprotein, while three antigens (?), often referred to as para-Lutheran, have limited evidence of belonging to the Lutheran system.

A

Lu11, Lu16, Lu17

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11
Q

• The ISBT designation of the Lutheran blood group system is

A

LU or 005.

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12
Q

• Allelic Codominant Genes: are, produced by allelic codominant genes.

A

Lua and Lub antigens

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13
Q

• Common Phenotypes: Most individuals express[?], while [?] phenotype is less common.

A

Lu(b)

Lu(a)

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14
Q

• Variable Expression: expression varies between individuals and even within an individual’s RBCs.

A

Lutheran antigen

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15
Q

strength has been confirmed to have low density
and variable expression.

A

Lub antigen

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16
Q

• Development: Antigens have been detected on fetal RBCs as early as [?], but they are poorly developed at birth and reach adult levels by age 15 years.

A

10 to 12 weeks of gestation

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17
Q

• Distribution: have not been found on platelets, lymphocytes, monocytes, or granulocytes.

A

Lutheran antigens

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18
Q

is widely distributed in tissues such as the brain, lung, pancreas, placenta, skeletal muscle, and hepatocytes, especially fetal hepatic epithelial cells.

A

Lutheran glycoprotein

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19
Q

Type: Most examples are IgM naturally_ occurring saline agglutinins. Some may also be IgA or IgG.

A

•Anti-Lua

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20
Q

Reactivity: They typically react better at room temperature than at 37°C, although some may react at 37°C by indirect antiglobulin test

A

Anti-Lua

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21
Q

are capable of binding complement, but in-vitro hemolysis has not been reported.

A

Anti-Lua

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22
Q

• Detection: often goes undetected in routine testing because most reagent cells are Lu(a).

A

Anti-Lua

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23
Q

It is more likely encountered as an incompatible crossmatch or during an antibody workup for another, specificity.

A

Anti-Lua

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24
Q

Experienced technologists recognize Lutheran antibodies by their characteristic loose, mixed-field reactivity in a test tube.

A

Anti-Lua

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25
Q

Effect of Enzymes: is not profoundly altered with common blood bank enzymes such as ficin and papain, but it can be destroyed with trypsin, chymotrypsin, pronase, AET, and DTT.

A

Anti-Lua

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26
Q

Most are clinically insignificant in transfusion.

A

Anti-Lua

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27
Q

There is one report of normal or near-normal survival of Lu(a) RBCs in a patient with

A

Anti-Lua

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28
Q

Immediate transfusion reactions due to are undocumented, and delayed reactions are rare and mild.

A

Anti-Lua

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29
Q

Hemolytic Disease of the Newborn (HDN): Because Lutheran antigens are poorly expressed on cord RBCs, cases of HDN associated with [?] are mild.

A

Anti-Lua

30
Q

Infants may exhibit weakly positive or negative direct antiglobulin tests and mild to moderate elevations in bilirubin.

A

Anti-Lua

31
Q

Many require no treatment, while others respond to simple phototherapy.

A

Anti-Lua

32
Q

In one report of mild HDN, the mother’s antibody titer rose to 4096.

A

Anti-Lua

33
Q

Although the first example of [?] was a room-temperature agglutinin, most [?] is gG and reactive at 37°C at the antiglobulin phase.

A

Anti-Lub

34
Q

IgM and IgA antibodies have also been noted.

A

Anti-Lub

35
Q

It is primarily made in response to pregnancy or transfusion.

A

Anti-Lub

36
Q

reacts with all cells tested except the auto-control, and reactions are often weaker with Lu(a-b-) RBCs and cord RBCs.

A

Alloanti-Lub

37
Q

Ficin or papain does not significantly alter reactivity.

A

Anti-Lub

38
Q

AET or DTT should destroy Lub antgen through disruption of the disulfide bond of the glycoprotein, but this may require optimal conditions.

A

Anti-Lub

39
Q

Autologous RBCs will test [?] if typing sera are available.

A

Lu(a)

40
Q

has been implicated with shortened survival of transfused cells and post-transfusion jaundice, but severe or acute hemolysis has not been reported

A

Anti-Lub

41
Q

Chromium survival studies demonstrate a rapid initial clearance of some Lu(b-) RBCs but much slower removal of those remaining

A

Anti-Lub

42
Q

may be regarded as clinically significant, but blood should not be withheld in emergency situations just because compatible units cannot be found

A

Anti-Lub

43
Q

is associated with only mild cases of HDN.

A

anti-Lua, anti-Lub

44
Q

This type of Lu(a-b-) phenotype is the result of a rare dominant regulator gene, which suppresses the expression of Lutheran antigens.

A

• Dominant In(Lu) Type

45
Q

Blood donor screenings have shown the frequency of this type of Lutheran null to be relatively rare.

A

• Dominant In(Lu) Type

46
Q

Individuals with this phenotype do not make anti-Lu3.

A

• Dominant In(Lu) Type

47
Q

In some families, the Lu(a-b-) phenotype demonstrates recessive inheritance, resulting from having two rare silent alleles at the Lutheran locus.

A

• Recessive Lulu Type

48
Q

Individuals with this phenotype truly lack all Lutheran antigens and can make an inseparable anti-Luab called anti-Lu3.

A

• Recessive Lulu Type

49
Q

This rare Lu(a-b-) phenotype, observed in a large Australian family, is thought to be the result of an X-borne inhibitor to Lutheran.

A

• Recessive X-Linked Inhibitor Type

50
Q

All Lu(a-b-) family members were male and carried trace amounts of Lub detected by adsorption-elution.

A

• Recessive X-Linked Inhibitor Type

51
Q

Lu(a-b-w) individuals with weakened Lutheran antigens, also known as Lu(w), may result from In(Lu) with a lesser degree of penetrance or an allele to In(Lu) that causes less suppression.

A

• Lu(w) Phenotype

52
Q

is a rare antibody that reacts with all RBCs except those testing Lu(a-b-).

A

Anti-Lu3

53
Q

It is usually antiglobulin-reactive.

A

Anti-Lu3

54
Q

This antibody is made only by Lulu individuals, i.e., the recessive type of Lu(a-b-).

A

Anti-Lu3

55
Q

It is associated with only mild cases of HDN.

A

Anti-Lu3

56
Q

RBCs from dominant and X-linked type Lu(a-b-) individuals can be safely transfused to patients with anti-Lu3.

A

Anti-Lu3

57
Q

Other Lutheran Antigens:

A

• Lu4, Lu5, Lu7, Lu12, Lu13, and Lu20
• Lu11. Lu16, and Lu17

58
Q

are antigens of very high incidence that are absent from Lu(a-b-) RBCs.

A

• Lu4, Lu5, Lu7, Lu12, Lu13, and Lu20

59
Q

They are located on the Lutheran glycoprotein and have not been shown to be inherited at the Lu locus.

A

• Lu4, Lu5, Lu7, Lu12, Lu13, and Lu20

60
Q

are high-incidence antigens phenotypically related to Lutheran but have not been shown to be located on the Lutheran glydoprotein nor have they been shown to be inherited.

A

• Lu11, Lu16, and Lu17

61
Q

The Lutheran (Lu) system comprises two major antigens, [?], giving rise to four possible phenotypes:
Lu(a+b-), Lu(a+b+), Lu(a-b+), and Lu(a-b-).

A

Lua and Lub

62
Q

Among these, [?] is the most common phenotype.

A

Lu(a-b+)

63
Q

• The genes encoding for the Lu antigens are linked to the

A

Se (secretor) genes

64
Q

• Both antibodies are rare.

A

anti-Lua, and anti-Lub

65
Q

react best at 37°C and often give a mixed field agglutination reaction

A

Lua

66
Q

react best at 37°C in the antiglobulin phase of testing.

A

Lub

67
Q

can cause mild hemolytic transfusion reactions (HTR), but they only rarely cause mild hemoiytic disease of the newborn (HDN)

A

• Lu antibodies

68
Q

[?] are often naturally occurring, while [?] typically develop after RBC stimulation by transfusion or pregnancy.

A

Lua antibodies

Lub antibodies

69
Q

may manifest as a naturally occurring saline agglutinin that reacts optimally at room temperature.

A

• Anti-Lub

70
Q

is typically an IgG antibody reactive at the antiglobulin phase

A

• Anti-Lub

71
Q

usually produced in response to foreign RBC exposure during pregnancy or transfusion.

A

• Anti-Lub

72
Q

is rare and may result from three different genetic backgrounds, including dominant In(Lu) type, recessive Lulu type, and recessive X-linked inhibitor type

A

Lu(a-b-)

Immunohematology Lec (35 decks)

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