Unformatted text preview: MLS 480 Clinical Immunohematology II Antigens/Antibodies Other Than ABO (Unit 2) Study Guide Objectives
: At the conclusion of this unit, the student will be expected to complete the following objectives with a score of 70% (grade of C) or better on course evaluations. Specifically, the student will be able to: a
1. Compare and contrast the blood group systems (P, I, H, Lewis, MNSsU, Kell, Duffy, Kidd, Lutheran, Xg
, high frequency antigens, HTLA, inherited polyagglutination cells, and Bg), with respect to: 2. Mode of inheritance 3. Antigens involved 4. Frequency of antigens 5. Antibody characteristics 6. Optimal conditions for antibody reactivity 7. Ability to cause HDN 8. Ability to cause HTR 9. Effect of enzymes 10. Appropriate enhancement techniques 11. Racial difference if significant 12. Biochemistry if related to blood groups 13. Clinical significance of antibodies 14. List the blood group systems that exhibit dosage effect 15. List the blood group system most effected by evanescence and the significance of this 16. Explain the mechanism and three antibodies frequently involved with extra vascular hemolytic (delayed) transfusion reactions 17. List several minor blood group system antigens Antigen/Antibodies other than ABO Study Guide 1.
Antibodies are expected to react at specific phases with their antigens. Name the antibodies for each a) phase below: (Include Rh, P, I, H, Lewis, MNSsU, Kell, Duffy, Kidd, Lutheran, Xg RT
P, I, H, Lewis, Lua
, M, N
Rh, S, s, U, Kell, Duffy, Kidd, Xga
, Lewis (sometimes) 2
List the 5 phenotypes of the P system: P
Identify the frequencies for the 2 most common P system phenotypes: Caucasian: P = 80%
P = 20% 1
For caucasian/AfricanAmerican: P = 94%
P = 6% 1
What are the detectable antigens for each of the P system phenotypes: P
Pk 1 1
Compare and contrast the precursor substance for the P1 antigen and the ABO antigens: Lactosyl ceramide is the precursor for ABO, Ii, Lewis, and P Lactosyl ceramide → pk → P → LKE Lactosyl ceramide → paragloboside → P antigen (same precursor as ABH) 1
The P system antigens are only glycolipids, not glycoproteins like the ABO, I and Lewis systems. 6.
Identify the antibody that can be inhibited by hydatid cyst fluid: Obj 1 AntiP 1 7.
Name the antibody and antibody class associated with paroxysmal cold hemoglobinuria (antibodies destroy RBCs when cold) and the test to identify it. Auto antiP IgG biphasic DonathLandsteiner test 8.
Describe the P system antibody most commonly associated with HDN and HTR: AntiP from P
individuals, most likely cold. 1
MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 1of 7 Revision Study Guide k
1 in pp individuals) can be IgG or IgM or both, RBC or NRBC stimulated, can cause HDN or HTR 9. What antigen in the P system deteriorates rapidly during storage? P antigen 1 10.
Briefly explain the transition of i to I antigen: There isn’t a gene for I or i. Absence of glycosyl transferases results in different sequences added to original structure. The I and i antigens are the subterminal portions of the molecules that are converted to H, A and B. The newborn ii is a straight chain oligosaccharide. Adult I is by the addition of branches off the original straight oligosaccharide. 11.
List the antibody characteristics of the Ii system: IgM only significant if it is masking the prsence of another antibody, not RBC stimulated, usually autoantibody. 12.
Identify the transient antibody associated with infectious mononucleosis: antii 13.
Distinguish between the I antibodies based on thermal activity: AntiI is a weak IgM. Strong antiI is a wide thermal range 30C or warmer. When patient cools, causes autoagglutination and vascular occlusions Raynaud’s Phenomenon or intravascular hemolysis. 14.
Name the antibody associated with Mycoplasma infections: antiI (cold agglutinin disease) 15.
Distinguish between antiI and antii based on cord blood activity: antiI DOES NOT agglutinate with cord cells antii agglutinates with cord cells 16.
Given lab data using 0 cord cells, 0 adult cells, and adult A
cells, distinguish between each of the 1
following: Hi HI A I (few H) 1
O cord O adult A adult 1
antiI 0 + + antiH + + 0 antiHI 0 + 0 antiA
0 0 + 1 17.
Describe what is unique about the acquisition of the Lewis antigens on RBCs: Lea
substance is produced if the patient has inherited the Le gene. This substance will adsorb onto the RBC surface and become an RBC surface antigen glycolipid Lea+b
substance interaction of the Le gene, the H gene and the Se gene. If all are present, the Leb
soluble antigen is produced in addition to Lea
, when both are in secretions. Leb
is better at adsorbing Leab+
If no Le gene is inherited, neither substance is produced and neither substance will attach to the RBC surface Leab
List the phenotypes and frequencies in the Lewis system: Le gene ~90%
Which of these people are secretors: Lea+b
Unknown MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 2of 7 Revision Study Guide Do enzymes affect the Lewis antigen? If so, how? Yes, enhance. Where are the Lewis antigens produced? Tissue 20.
Compare and contrast the precursor substance for the Le antigen and the precursor and its substance for the ABO antigens: Le has two Fuc one off Gal, one off Galnac ABO precursor just has the one Fuc off of the Gal a
21. Discuss the significance of the following antibodies: antiLe
, antiLe Neutralized by Lewis substances, poor attachment to RBCs and of the IgM class 22. Do the lewis antigens show dosage and are the reactions changed with enzymes? No dosage, enhanced by enzymes 23. What is the Bg antigen? Residual MHC1 on RBC surface 24.
Compare and contrast the MNSsU system with respect to: Antigens:
Mode of inheritance: MNSs
U Chromosome: 4 Antigens involved: MN codominant Ss codominant U on S structure Dosage: Yes Enzyme reaction: Decreased with enzymes When developed:
Developed at birth Frequency: (exact numbers are not necessary just range) White
MN glycophorin A
SsU glycophorin B Antibodies: AntiM Antibody class
: naturally occuring IgM or immune IgG Complement fixation
: No Temp of reactivity
: No reaction above 30C not clinically significant Ability to cause HDN/HTR
: if reacting at 30C and IgG should be concerned RBC stimulated
? No AntiN Antibody class: IgM or occ IgG N antigen is commonly seen as self Complement fixation
: No Temp of reactivity
: only significant if reacting above 30C Ability to cause HDN/HTR:
No RBC stimulated
? No AntiS Antibody class
: IgG, occ IgM Complement fixation
: Poorly Temp of reactivity
: 37C and AHG Ability to cause HDN/HTR
: Yes MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 3of 7 Revision Study Guide RBC stimulated?
Yes Anti s Antibody class
: IgG Complement fixation
: Poorly Temp of reactivity
: 37C and AHG Ability to cause HDN/HTR: Yes RBC stimulated?
Yes 25.Compare and contrast the Kell system with respect to: Antigens:
Mode of inheritance:
Kpa Kpb Jsa
Jsb Antigens involved
: K Kell → very high antigenicity k cellano → high antigenicity Frequency: K 9% k
99% Kpa 2% Kpb 99.9% Jsa
0.01% 20% Black Jsb
: occasionally When developed
: Developed at birth Enzyme Reaction
: No change decrease AET and ZZAP What is the McLeod phenotype and syndrome? Rare lacks K and K
, xlinked patients have muscle and nerve disorders x
m Antibodies: AntiK Antibody class
: IgG Complement fixation
: Yes, seldom to lysis Temp of reactivity: AHG Ability to cause HDN/HTR
RBC stimulated? Yes Rare antibodies antibodies to Kpa
other low frequency antigens antidbodies to k, Kpb
other high frequency antigens Antibody class: IgG Complement:
Warm, AHG HDN and HTR
: Yes 26. Compare and contrast the Duffy Blood Group System with respect to:
Antigens involved and frequency: Caucasian
91% chinese Dosage: Yes MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 4of 7 Revision Study Guide When developed: Birth nzyme Reaction
: Decreased Relationship to Rh:
Fy6 Antibodies: Antibody class: IgG Complement fixation
: Yes, but not to lysis Temp of reactivity
: AHG Ability to cause HDN/HTR
: Yes RBC stimulated?
Yes What is the antigen inheritance and significance of Fy(ab) in the black population
68% which gives them resistance to
Compare and contrast the Kidd Blood Group System with respect to: Antigens: a
Rare When developed: Birth Dosage: Yes Enzyme activity
: Increased Antibodies: Antibody class
: IgG Complement fixation
: Yes, well Temp of reactivity
: AHG Ability to cause HDN/HTR: yes RBC stimulated?
Yes Why is this a particularly problematic antibody (evanescent) and what is the possible problem with the antibody screen? antiJka
fade from circulation and if stimulated make an anamnestic response with delayed intravascular and extravascular hemolysis. May be missed in the screen because of low quantity in circulation What population are you most like to find Jk (ab)? Polynesians/Far East 28.
Compare and contrast the Lutheran Blood Group System with respect to: Antigens:
Mode of Inheritance
: Antigens involved:
Lub Frequency: 8%
99% Dosage: Yes When developed:
Poor at birth Enzyme Reaction
: No effect Antibodies: a
AntiLu Antibody class: IgM, rare IgG Complement fixation: Yes, but not to lysis Temp of reactivity
: RT MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 5of 7 Revision Study Guide 31. Ability to cause HDN/HTR: No or very mild RBC stimulated?
AntiLu Antibody class
: IgM/IgG Complement fixation
: occ Temp of reactivity: 37/AHG Ability to cause HDN/HTR:
Yes/mild RBC stimulated?
What system does the Miltenberger system belong to: MNSs 30.
Name the blood group system associated with chronic granulomatous disease: McLeod phenotype and syndrome Identify the Rh antigen frequencies in terms of % of compatible blood for a patient with Rh antibodies: Anti: D
a. Identify the chromosome location of the Xg
gene: X b. Explain the genetics of the antigen:
Only blood group on the X chromosome c. List the phenotypes and frequencies: Xga
89% of females, 67% of males a
d. Describe the antibody characteristics of AntiXg
IgG, AHG phase reactivity, Yes binds complement, but not to lysis, no HDN/HTR, destroyed by enzymes, RARE 33.
High Frequency Antigens: a. Define high frequency antigens: antigens that most of the pop. have a
b. Identify the major blood group system with which the En
antigen is associated:
MNSs c. Explain why it is so difficult to find blood for a patient with antibodies to this system: Rare units without antigen 34.
High Titer Low Avidity Antibodies (HTLA):
High titer >64 reactivity, but low avidity for agglutination when binding antigen (weak reactions) a. List 4 characteristics of HTLA antibodies: IgG, AHG phase, titer >64, poor agglutination, clinically insignificant, react poorly with LISS b. Name all antigens that are defined as HTLA antigens: Chido, Rodgers, Knops, McCoy, York, Cost c. Identify what is unique about Chido and Rodgers antibodies: Neutralized/inhibited by plasma containing C4d 35.List four forms of inherited poly agglutination Cad
NOR 36.List a non red blood cell stimulated antibody in the Rh group AntiCw
AntiE 37.Glycophorin B is the structure for which antigen? SsU 38.What transferase converts the precursor molecule to an H molecule? Fucosyl transferase 39.What three IgG antibodies are the most likely to cause an extravascular (delayed) transfusion reaction? Kidd
Duffy MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 6of 7 Revision Study Guide Antibody Class Temp Phase Fya IgG Warm AHG Fyb IgG Warm AHG Jka IgG Warm AHG Jkb IgG Warm AHG P IgM Cold IS PI IgM Cold IS M IgM Cold IS N IgM Cold IS Lea IgM Cold IS Leb IgM Cold IS Lua IgM Cold IS Lub IgM Cold IS S IgG Warm AHG H IgM Cold IS D IgG Warm AHG C IgG Warm AHG E IgG Warm AHG MLS 480 Clinical Immunohematology II
2012 RPaur Antigen / Antibodies other than ABO Page 7of 7 Revision Study Guide ...
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- Summer '16
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- Biology, blood group, Antigen / Antibodies, Clinical Immunohematology