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CCHS SBB > Polyagglutination > Flashcards

Polyagglutination Flashcards

1
Q

polyagglutination

A

red blood cells that agglutinate in the presence of virtually all adult serum

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2
Q

polyagglutination cause

A

altered red blood cells exposing an antigen that is normally hidden from the immune system

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3
Q

classifications of polyagglutination

A

microbial and non-microbial

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4
Q

microbial polyagglutination examples

A

T, Th, Tk, Tx, acquired B, VA

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5
Q

non-microbial polyagglutination examples

A

Tn, Cad, HEMPAS, hemoglobin M

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6
Q

microbial polyagglutation cause

A

bacterial enzymes removing carbohydrates normally present on red cells and exposing new antigens

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7
Q

non-microbial polyagglutination cause

A

abnormal synthesis of red blood cell membrane structures

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8
Q

T polyagglutination/T activation

A

neuraminidase action cleaves N-acetylneuraminic acid residues terminally from RBC membrane glycolipids and glycoproteins, causing subterminal T receptor to be exposed. Binds with IgM anti-T

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9
Q

Th polyagglutination

A

incomplete or intermediate form of T activation; weakened expression or early form of T polyagglutination

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10
Q

bacteria involved in Th polyagglutination

A

Bacteroides, Clostridia, E. coli, Proteus

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11
Q

bacteria involved in T polyagglutination

A

Clostridium perfringens, pneumococci, Vibrio cholerae, flu virus

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12
Q

Tk polyagglutination

A

microbial beta-galactosidases cleave a galactose residue from para-globoside, exposing N-acetylglucosamine

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13
Q

polyagglutination associated with kids with pneumococcal infections

A

Tk

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14
Q

bacteria involved in Tk polyagglutination

A

Bacteroides fragilis, Aspergillus niger, Candida albicans, Serratia

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15
Q

polyagglutination that results in altered expression of ABH, Ii, Lewis, P1 antigens

A

Tk

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16
Q

Tx polyagglutination

A

caused by unidentified bacteria, seen in kids with pneumococcal infections, mechanism not fully understood

17
Q

polyagglutination in which H antigens are depressed significantly

A

VA

18
Q

Tn polyagglutination

A

caused by somatic mutation in faulty hematopoietic stem cell clone

19
Q

polyagglutination associated with myelodysplastic syndromes and acute leukemia

A

Tn

20
Q

polyagglutination with mixed field agglutination

A

Tn

21
Q

polyagglutination that results in incomplete structure on MN antigen

A

Tn

22
Q

inherited permanent polyagglutination forms

A

HEMPAS, Cad, NOR, hemoglobin M-Hyde Park

23
Q

HEMPAS

A

hereditary erythroblastic multinuclearity with positive acidified serum

24
Q

polyagglutination with increased amounts of I and i antigens, decreased H antigen

A

HEMPAS

25
Q

polyagglutination with increased susceptibility for complement lysis

A

HEMPAS

26
Q

positive acidified serum test confirms presence of ___ polyagglutination

A

HEMPAS

27
Q

polyagglutination that has considerable resistance to Plasmodium falciparum invasion

A

Cad

28
Q

polyagglutination agglutinated by anti-Sda

A

Cad

29
Q

polyagglutination with positive reaction to Dolichos biflorus lectin

A

Cad

30
Q

polyagglutination associated with P blood group system

A

NOR

31
Q

inherited form of polyagglutination that has been identified in South African families

A

hemoglobin M-Hyde Park

32
Q

cause of Hemoglobin M-Hyde Park polyagglutination

A

reduction in sialylation of O-linked oligosaccharide chains on membrane components of M-Hyde Park; heterogeneity of the molecular size of SGP’s

33
Q

why is polyagglutination no longer seem in routing blood banking?

A

monoclonal antisera replaced human ABO forward typing reagents and antiglobulin reagents; lack naturally occurring polyagglutinins that are found in human adult serum

34
Q

transfusion protocols for T-activated polyagglutination patients

A

washed or plasma reduced red cells and platelets, low anti-T titer plasma

35
Q

enzyme treatment of polyagglutinable cells

A

Tk, Cad, NOR enhanced
Th, Tn destroyed
T, VA, HEMPAS not affected

36
Q

polyagglutination should be suspected if:

A

agglutination with group AB adult sera
no agglutination with cord sera
no agglutination with patient’s own serum
negative direct Coombs

CCHS SBB (40 decks)

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