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BB Week 2
ABO-Rh, Antigens, and Antibodies
| Question | Answer |
|---|---|
| Differentiation of A1 vs A2 subgroups | Dolichos biflorus or human anti-A1 (reacts with A1 but not A2) |
| hh Phenotype | Bombay Phenotype (Oh) |
| T/F: Bombay patients will type as O despite genotype | True |
| T/F: Bombay patients can receive O blood | FALSE. They will DIE. Can only receive other Bombay blood. |
| Blood types with least amount of H | A1B and Oh |
| Blood types with most amount of H | O and A2 |
| Amounts of H per blood type | O > A2 > B > A2B > A > A1B > Oh |
| Test to differentiate between O and Oh phenotypes | Anti-H lectin (Ulex europaeus) |
| Se gene allows for expression of __ antigens in body fluids | A, B, H, Leb |
| T/F: Se is needed for Lea to be expressed on saliva | False. Se is needed for H to be expressed on saliva but not Lea. |
| Testing for B subgroups | Bandeiraea simplicifolia lectin |
| When seal is broken, expiration of products becomes... | Products stored at 1-6C: 24 hours; Products stored at RT: 4 hours |
| T/F: A2 subgroups look normal on forward and reverse type, unless patient develops anti-A1 | True |
| T/F: A1 has more H antigenic sites than A2 | False. A1 is more efficient in converting H to A than A2 is. |
| T/F: Most of the population are Secretors | True, 80% of the population are Secretors |
| Secretor test with saliva and blood | 1) Antisera and saliva are mixed. 2) If pt is a secretor, antisera and saliva will bind. 3) Mix blood in. 4) Secretors will not agglutinate due to already having complexes form, while nonsecretors will agglutinate. |
| Cold (IgM) antibodies | ABH, I/i, Lewis, M, N, P1, |
| Could be IgM or IgG | M and N |
| Warm (IgG) antibodies | Kell, S/s, Duffy, Kidd, Rh |
| Destroyed by enzymes | MNS, Duffy |
| Le antigens | Plasma antigens that absorb onto RBCs and can appear in body fluids and saliva |
| If someone has Le and H but NOT Se | Lea will be on RBCs and saliva. Leb and H will be on RBCs only. |
| Interpretation of mini cold panel using reagent RBCs: AB = pos, O = pos, Cord O = neg, AC = pos | Anti-I |
| Interpretation of mini cold panel using reagent RBCs: AB = pos/neg, O = pos, Cord O = pos/neg, AC = neg | Unexpected cold anti |
| Interpretation of mini cold panel using reagent RBCs: AB = pos, O = neg, Cord O =neg, AC = neg | Anti A or B |
| Agglutination | Antibody reactivity |
| Aggregation | Rouleaux |
| Rosenfield for: D, C, E, c, e | D = 1, C = 2, E = 3, c = 4, e = 5 |
| Fisher-Race | System that uses D, C, E, c, e to denote Rh antigens |
| Wiener | System that uses R, r, R1, R2, Rz, r', r", rz to denote Rh antigens |
| DCE | Rz |
| Dce | R0 |
| DCe | R1 |
| DcE | R2 |
| dCE | ry |
| dce | r or 0 |
| dCe | r' |
| dcE | r" |
| Rh antigens are integral to membrane activity. Therefore, Rh null individuals have... | Intravascular hemolysis |
| Hierarchy of immunogenicity of Rh antigens | D > c > E > C > e |
| True or False: Rh neg donors need to have Weak D performed | True |
| Weak D is ___ at RT but is ___ at AHG | Negative, positive |
| Patients who need to be Weak D tested | Rh neg babies born to Rh neg moms |
| D control is needed for | AB+ or any ABO with Rh neg at RT |
| Most common cause for a positive Weak D control | Positive DAT |
| Prevalence of dCE, dCe, dcE, DCE | Rare |
| Acquired B | E coli 086; individuals with colon or GI cancer have increased permeability, allowing microbial polysaccharides to seep into bloodstream and have RBCs absorb antigen |
| Group I ABO discrepancies | Weak or missing reverse |
| Group II ABO discrepancies | Weak or missing forward reactions; may be caused by A or B subgroups (don't strongly type with antisera), Leukemia's or Hodgkin's disease, Acquired B |
| Group II ABO discrepancy resolution | 1) Acidify anti-B reagent to pH 6; 2) Run DAT; 3) Run AC |
| Group III ABO discrepancies | Excess reactions in reverse caused by rouleaux (causes: increased globulins, fibrinogen, Wharton's jelly) |
| Group IV ABO discrepancies | Misc, caused by cold auto or allo antis, transfusions |
| Lewis antigens | Carbohydrate blood group that absorbs on to RBCs |
| True or False: Lea and Leb are antithetical genes | False, they arise from interactions from Le and Se genes |
| True or False: Lewis antigens are found on cord cells | False |
| Nonsecretors | Le(a+b-) |
| Secretors | Le(a-b+) |
| Most adults are secretors or nonsecretors? | Secretors |
| Null Lewis phenotype | Le(a-b-) |
| Groups that are often Lewis null | Babies, sometimes pregnant women |
| Weak secretors | Le(a+b+) (Rare, more common in Asians) |
| Le gene | FUT3 |
| Se gene | FUT2 |
| I and i antigens | Carbohydrate chains that are expressed reciprocally with age |
| Anti-I | Naturally occurring autoanti found in almost all sera |
| i adults | Rare; associated with anemia, thalassemia, sicel cell, PNH, HEMPAS, cataracts |
| # Units needed to be antigen typed | Express % antigen negative blood in general pop as decimal: # Units needed * Antigen1 neg * Antigen2 neg, etc. |
| P antigen | Takes up to 7 years to be expressed, deteriorates with storage |
| Antibody associated with Echino granulosus tapeworms | Anti-P1 |
| P1 phenotype reacts with | Anti-P1 and anti-P |
| P2 phenotype reacts with | Anti-P |
| P null or p phenotype | Rare but is more common in Japan, Sweden and Amish communities. Doesn't react with any P anti BUT produces Anti-Tja or PP1PK |
| Anti-Tja or PP1PK | Produced by P null. Large thermal range and is IgM AND IgM. Associated with HDFN, transfusion reactions, and spontaneous abortions. |
| Associated with PCH, viral infections, and syphilis | Autoanti-P |
| Autoanti-P | Biphasic IgG cold auto |
| M and N antigens | Found on ends of glycophorin A (GPA) on RBCs and are easily degraded by enzymes |
| S and s antigens | Located further down on glycophorin B (GPB) on RBCs and are more resistant to enzymes |
| Anti-M and Anti-N | IgM or IgG but doesn't bind complement either way; not clinically significant as long as it's nonreactive at 37 |
| Anti-S and Anti-s | IgG and reactive at 37, can bind complement and cause HDFN and transfusion reactions |
| K antigen prevalence | 9% |
| Is anti-k common or rare? | VERY rare; only 2 in 1000 lack antigen |
| McLeod syndrome etiology | Absence of XK protein, which the Kell glycoprotein usually links to, creating the Kx antigen. |
| McLeod syndrome presentation | All males, acanthocytic RBCs with decreased survival, chronic compensated anemia, muscle and nerve disorders (muscle dystrophy progressing to cardiomyopathy, areflexia, choreiform movements) |
| Fy(a-b-) prevalence | 70% African descent. Resistant to malaria! |
| Fya(a+b-) prevalence | 90% Asians |
| Fya(a+b+) or Fya(a-b+) prevalence | Most common phenotypes in whites |
| Duffy antibodies | Usually IgG and react best at AHG, acute and delayed transfusion reactions, may show dosage, HDFN, don't react with enzyme treated RBCs |
| An Fy(a-b-) patient is exposed to Fy(a+b+) blood but doesn't develop an antibody. Why is that? | Black Fy(a-b-) patients still express Fyb in tissues, so they don't develop an antibody. Not true for whites. |
| Jk(a-b-) phenotype | Difficulty in concentrating urine since the antigens are urea transporters. Usually Asian. |
| Kidd antigens (Jka and Jkb) | Found on the RBCs of most people and are urea transporters. Reactions grow STRONGER with papain or ficin. |
| Kidd antibodies | Titers rise and fall rapidly. Associated with delated transfusion reactions. |
| Lutheran (Lua and Lub) antigens | Poorly developed at birth and rarely causes HDFN |
| T/F: Anti-Lub is very rare since it's such a low prevalence antigen | FALSE. It's a very rare antibody because almost everyone (99%) has the antigen. |
| Anti-Lua is IgG or IgM? | IgM |
| Anti-Lub is IgG or IgM? | IgG |
| IAT Steps | 1) Antibody attaches to antigen at 37C. 2) Excess antibody is washed away. 3) Add AHG 4) Spin and watch for reaction. 5) Add CC to negative cells |
| T/F: Not washing the cells after the 37C step will cause extra reactivity to be seen in an IAT. | FALSE. Unbound antibody will neutralize the reagent, causing a FALSE NEGATIVE. This is why CC are added to negative tubes. |
| Enhanced with enzyme treatment | Kidd, I, P, Lewis, Rh |
| Destroyed with enzyme treatment | Duffy, M, N, S, s |
| Shows dosage | Kidd, Fy, Rh, M, N, S ("KIDDS and DUFFY the MONKEY (Rh) eat lots of M and Ns.") |
Created by:
rachelkayw