Polyagglutination

Question 1

Polyagglutination

Answer 1

Red Blood Cells that agglutinate in the presence of virtually all adult human serum. An RBC abnormality not a plasma abnormality. consequence of a change from normal that occurs on the surface of the red cell. Not related to blood group specificity \1024797639\

Question 2

Cryptantigen

Answer 2

crypt=hidden, exposeure of an antigen that is normally hidden (T, Th Tk, Tx)

Question 3

Exposure of Cryptantigen

Answer 3

Happens most often as a result of bacterial infection. Bacterial enzymes remove carbohydrates normally present exposing new antigens. Most normal human adults have naturally occurring IgM that are reactive with cryptantigens. (T, Th Tk, Tx)

Question 4

Microbial Polyagglutination

Answer 4

Bacterial enzymes remove carbohydrates normally present exposing new antigens

Question 5

Non-Microbial Polyagglutination

Answer 5

Abnormal synthesis of RBC membrane structures (Tn, Cad, HEMPAS, Hemoglobin M (Hyde Park) Tr

Question 6

Glycophorin structure

Answer 6

Sugars are added onto the amino acids

Question 7

T polyagglutination

Answer 7

“T activation” Cleaving Enzyme=neurominidase. Bacteria or viruses infecting the individual produce the enzyme and cleaves NEuNac and therefore decreases the amount of sialic acid

Question 8

Most common bacteria associated with T activation

Answer 8

Clostridium perfringes, Vibrio Cholorae, streptococcous pneumoniae

Question 9

Most common type of polyagglutination

Answer 9

T activation

Question 10

Cad

Answer 10

Inherited autosomal dominant. Cad+ cells strong expression of Sda also called Super Sda. Resistant to plasmoidum falciparum, react strongly with anti-Sda which is naturally occurring in most human sera.

Question 11

Th Polyagglutination

Answer 11

Low level/early/mild T activation- same biochemical mechanism as T activation- neuraminidase cleaves NeuNac- not an effective removal therefore normal levels of sialic acid are present. May be a pre-leukemic marker. Lacking B-3-D-Galactosyltransferase.

Question 12

Tx and VA polyagglutination

Answer 12

mechanisms are not fully understood but know the terms

Question 13

Tk Polyagglutionation

Answer 13

Cleaving enzyme= Beta-galactosidase (endo or exo)- cleaves the Gal-GlcNac linkages found primarily on paragloboside structures and ABH/Ii precursors. Decreased expression of ABH, Lewis, Ii and P1 antigens

Question 14

Acquired B Polyagglutination

Answer 14

Cleaving enzyme=deacetylase- causes deacaetylation of group A immunodominant sugar- leaves galactosamine, cross reactivity that makes the A antigen appear like a B antigen in tube testing

Question 15

Tn polyagglutination

Answer 15

Persistent mixed field polyagglutination- persisitent= due to somatic mutation of hematopoietic stem cells . Tn antigen is found on the same structures as the T antigen (Glycophorin A and B) Mutated clone of cells lack beta-3-galactosyltransferase. MF is due to two different cell populations 1 being mutant clone 2. being normal

Question 16

Chromosomal mutation of Tn polyagglutionation

Answer 16

Gene carried on the X chromosome

Question 17

HEMPAS

Answer 17

Hereditary Erythroblastic Multinuclearity witeh a Positive Acidified Serum Test . Inherited autosommal recessive, RBCs have a second membrane internal and parallel to the external membrane, The RBCs react with Anti-I anti-i and Glysine soja

Question 18

Ham’s test

Answer 18

Positive Acidified Serum Test, used in diagnosis of PNH. Placing RBCs in a mild acid-hemolysis (increased RBC fragility) indicates PNH or congenital dyserythropoietic anemia (HEMPAS), not widely used anymore.

Question 19

Tr Polyagglutination

Answer 19

Mmebrane proteins are not glycosylated, inherited autosomal recessive

Question 20

Hemoglobin M-Park Polyagglutination

Answer 20

Reported in a south african family of mixed race, due to 2 unrelated RBC membrane abnormalities

Question 21

Today vs. Historical detection of polyagglutination

Answer 21

Used to use human derived serum, abo discrepancy, positive dat and minor crossmatch. Today: monclonal antisera lack the naturaly occurring polyagglutinins that are found in adult human sera.

Question 22

Today vs. Historical detection of polyagglutination

Answer 22

Used to use human derived serum, abo discrepancy, positive dat and minor crossmatch. Today: monclonal antisera lack the naturaly occurring polyagglutinins that are found in adult human sera. May be detected with IS crossmatch, same donor incompatibilities or MF due to Tn polyagglutination.

Question 23

How are different types of polyagglutination classified in lab tests

Answer 23

Through the use of Lectins,

Question 24

Polybrene vs. Glycine Soja

Answer 24

Polybrene- sialic acid deficient RBCs will not aggregate. Glycine Soja- sialic acid deficient RBCs strongly react

Question 25

Enzyme treatment of RBCs with papain or ficin

Answer 25

Increased reactivity Tk, Cad. Decreased reactivity Tn and Th. No change- T, VA, HEMPAS

Question 26

Lectins

Answer 26

Proteins found in plants and seeds, invertebrate animals and lower vertebrates. Reactivity depends on the terminal of subterminal sugars and their 3d configuration

Question 27

Transfusion practices for polyagglutination

Answer 27

Cellular products: cell saver or Saline washed products. Plasma- avoidance!! Plama from a suitable donor T/Tn deficient Needs a minoR crossmatch- Donor plasma and recipient RBCs

Question 28

Tn cells react with what lectins?

Answer 28

Dolichos Bifloris, Glycine soja (max) Salvia sclarea, Salvia hominum Griffonica simplifica 1

Question 29

Cad cells react with what lectins?

Answer 29

Dolichos Bifloris, Glycine Max, Salvia hominum

Question 30

Tk cells react with what lectins?

Answer 30

(TAKITAKI) -Arachis Hypogaea, Griffonica simplifica II

Question 31

T cells react with what lectins?

Answer 31

(TAG) arachis hypogaea, glycine soja

Question 32

Th

Answer 32

(THA) Th- archais hypogaea

Question 33

Cad+ with lectins

Answer 33

positive with salvia hominum and glycine soja (CADSG)