| Question | Answer |
| K | Kell; 9%+; 37 AHG |
| k | Cellano; 99.8%+; 37 AHG |
| Kpa | Penney; 2% Caucasians; overall low frequency; 37 AHG |
| Kpb | Rautenberg; >99.9%+; 37 AHG |
| Jsa | Sutter; 20% African Americans; <0.1% Caucasians; overall low frequency; 37 AHG |
| Jsb | Matthews; >99%+; 37 AHG |
| Name the high frequency Kell antigens | Cellano, Rautenberg, Mathews |
| Name the low frequency Kell antigens | Penney, Sutter |
| Name the Kell antigens | Kell=K, Cellano=k, Penney=Kpa, Rautenberg=Kpb, Sutter=Jsa, Matthews=Jsb |
| What Ig class are Kell antibodies in? | IgG (some are IgM in early detection) |
| Do Kell antibodies fix complement? | 20% bind complement |
| Is Kell implicated in HDN and HTR | Yes-sever |
| Where does anti-Kell rank in immunogenicity? | Next after ABO and RH |
| Is the McLeod phenotype a male or female problem? | Male |
| What Kell antigens have decreased expression in McLeod phenotype? | k-Cellano, Jsb-Matthews, Kpb-Rautenberg |
| What disease is linked to the McLeod phenotype? | X-linked chronic granulomatus disease (CGD). Granulocytes can ingest bacteria but not kill them. |
| What are some RBC and physical abnormalities in McLeod phenotype and CGD? | Acanthocytosis (thorny), Anisocytosis, increased osmotic fragility, reticulocytosis, reduced serum haptoglobin, spleenomegaly; cardiomyopathy, increased CK-MM bands |
| What blood group do enzymes make go away? | "D"uffy "M"a"N"u"S"cript. Sometimes little s |
| Name the phenotypes and frequencies of the MN blood group: | Genotype MM = Phenotype M 28%; Genotype MN = Phenotype MN 50%; Genotype NN = Phenotype N 22% |
| In what Ig class are MN antibodies? | IgM, most are cold reactive. There are a few IgG |
| What reaction temperature and medium do MN antibodies react? | IS; room temperature or lower |
| Do M or N antibodies fix compliment? | No |
| Are M or N antibodies implicated in HDN or HTR? | Rare |
| At what pH do M and N antibodies best react? | 6.5 |
| Do M and N antibodies show dosage? | Yes, MM is stronger than MN and NN is stronger than MN (I think. What do you think Josh?) |
| Are M and N antibodies destroyed by enzymes? | Yes |
| Does S antibody fix complement? | Yes |
| Is S antibody implicated in HDN and HTR? | Severe HTR, yes HDN |
| Does S antibody show dosage? | No |
| Is S antigen destroyed by enzymes? | S yes (ficin and papain), little s maybe |
| Describe the formation of anti-U: | Formed in S-s-U- individuals |
| Is anti-U implicated in HDN and HTR? | Yes |
| Name the four phenotypes of the Duffy system and their frequencies: | Fy(a+b-) Caucasian 18%, African American 0.9%; Fy(a+b+) Caucasian 49%, African American 1.3%; Fy(a-b+) Caucasian 34%, African American 22%; Fy(a-b-) Caucasian 0.01%, African American 68% |
| What is the frequency of Fy(a+b-) among Caucasians and African Americans? | Caucasian 18%, African American 0.9% |
| What is the frequency of Fy(a+b+) among Caucasians and African Americans? | Fy(a+b+) Caucasian 49%, African American 1.3% |
| What is the frequency of Fy(a-b+) among Caucasians and African Americans? | Caucasian 34%, African American 22% |
| What is the frequency of Fy(a-b-) among Caucasians and African Americans? | Caucasian 0.01%, African American 68% |
| How do the Duffy antigens rank in immunogenicity as compared to other blood group systems? | Modestly immunogenic |
| Do Duffy antibodies fix complement? | Yes |
| Are Duffy antibodies implicated in HDN and HTR? | Yes HDN, delayed hemolytic |
| Do Duffy antibodies show dosage? | Yes |
| Are Duffy antibodies destroyed by enzymes? | Yes |
| Describe the relationship of the Duffy antigens and Plasmodium vivax (malaria): | Fy(a-b-) phenotype shows resistance to malaria infection. Merozites can only invade Fy(a+) or Fy(b+) cells with normal antigens present. (Survival of the fittest example) |
| Describe the four phenotypes on the Kidd system and their frequencies: | Jk(a+b-) Caucasian 26.3%, African Am 51.1%, Asian 23.22%; Jk(a+b+) Caucasian 50.3%, African Am 40.8% Asian 49.94%; Jk(a-b+) Caucasian 23.4%, African Am 8.1%, Asian 26.84%; Jk(a-b-) Caucasian <0.01%, African Am <0.01%, Asian 0.9 to <1% |
| Do Kidd antibodies fix complement? | Yes, best to use polyspecific AHG to detect |
| Are Kidd antibodies implicated in HDN and HTR? | Mild HDN, Delayed HTR |
| Do Kidd antibodies show dosage? | Yes |
| Name three reasons the Kidd system is hard to work with in the Blood Bank? | Shows dosage. Found in combination with other antibodies. Weak reactions. Kidds are always late!!! |
| Name the two antigens in the Lutheran system and their frequencies: | Lua 8%; Lub 99.8% |
| What is the difference between anti-Lua and anti-Lub? | Anti-Lua is seen occasionally, but anti-Lub is very rare as most people are positive (high frequency Ag). |
| Do the Gerbich antibodies fix complement? | Rarely |
| Are the Gerbich antibodies implicated in HDN and HTR? | Mild HDN and HTR |
| Name the 3 main antigens in the Gerbich system: | Ge2, Ge3, Ge4 |
| Are the Diego antibodies implicated in HDN and HTR? | Mild rare HDN |
| Name the 2 main antigen pairs in the Diego system: | Dia, Dib and Wra, Wrb |
| Name the antigen in the Xg system: | Xga |
| Are Xg antibodies implicated in HDN and HTR? | None documented |
| What Ig class are the Scianna antibodies in? | IgG and some naturally occurring IgM |
| What is the reaction temperature and medium for Scianna antibodies? | AHG (or RT of IgM) |
| Are the Scianna antibodies implicated in HDN or HTR? | HDN |
| Name the 2 main antigens in the Scianna system: | Sc1 and Sc2 |
| Name the 2 main antigens in the Cartwright system: | Yta and Ytb |
| Are the Cartwright antibodies implicated in HDN or HTR? | Subclinical HDN |
| Are the Dombrock antibodies implicated in HDN and HTR? | Mild or subclinical HDN |
| Name the 5 main antigens in the Dombrock system: | Doa, Dob, Hy, Gya, and Joa |
| There are 11 antigens in the Cromer system; 8 are high incidence; name them: | Cra, Tca, Dra, Esa, WESb, UMC, IFC, and GUT1 |
| There are 11 antigens in the Cromer system; 3 are low incidence; name them: | Tcb, Tcc, and WESa |
| Are Cromer antibodies implicated in HDN and HTR? | Yes, HTR, no HDN |
| What Ig class are the Chido/Rodgers antibodies? | Complement C4 component adsorbed onto RBC membrane |
| What is the best reaction temperature and medium for Chido/Rodgers antibodies? | Polyspecific AHG |
| Are Chido/Rodgers antibodies implicated in HDN and HTR? | No HTR, but anaphylactic reactions |
| Name the 2 main antigens in the Chido/Rodgers system and why they are so different: | Ch and Rg are part of the 4th component of Complement, and are adsorbed on to RBC membranes. They are seen as anaphylactic reactions of complement deficient persons. |
| What makes an antigen be known as a high incidence antigen? | 99% of the population or greater have it |
| Name several examples of high incidence antigens: | Vel, Lan, Ata, Jra, Sda |
| What makes an antigen be known as a low incidence antigen? | Less than 1% of the population has it |
| Name several examples of low incidence antigens: | Batty, Christiansen, Biles, Box, Torkildesen, Peters, Reid, Jensen, Livesay, Milne, Rasmussen, Oldeide, Katagiri, SARA and Reit |
| There are seven parts of a complete Compatibility Test. List the first 4: | 1. Positive ID of patient and sample; 2. Review of Pt's history/records; 3. ABO & Rh type of patient; 4. Screening pt's serum/plasma for unexpected RBC antibodies |
| There are seven parts of a complete Compatibility Test. List the last 3: | 5. Confirmation of ABO Group & Rh type of donor units; 6. Major serologic crossmatch between donor RBCs and patient's serum/plasma or computer crossmatch; 7. Labeling of products with patient's information |
| List 4 Blood Groups that are known to cause hemolysis: | ABO, P, Lewis, Kidd, and Vel systems |
| Why is patient identification such an integral step in Blood Transfusion? | If the patient is not correctly identified prior to obtaining the sample, an incorrect blood type may be obtained or an antibody present may be missed. These could result in death of the patient following transfusion. |
| The Antiglobulin Test: What is the purpose of the AGT? | To detect bound IgG and/or Complement on the red blood cells. |
| Antiglobulin Test: Name 3 types of AHG reagent: | Polyspecific (IgG and C3d), Monospecific IgG and Monospecific C3d |
| Antiglobulin Test: How does AHG work? | Any cell coated with Ab will be complexed with AHG, and the clumps will form- macroscopic or microscopic |
| Antiglobulin Test: Name the 2 types of AHG test, and which is in vivo vs. in vitro: | DAT-direct Antiglobulin test- detects in vivo coating of Ab; IAT- indirect Antiglobulin test- detects in vitro coating of Ab onto cells |
| Antiglobulin Test: What is the purpose of the 2 AHG tests? | DAT: In vivo….IAT: In vitro |
| Describe "unexpected antibodies" | Antibodies to red cell antigens that are not expected (other than ABO antibodies) |
| What is the purpose of the antibody screen? | To detect unexpected red cell antibodies in the patient's serum or plasma |
| What type of cells are used in antibody screening and identification? | Group O, RH positive and negative |
| What are enhancement reagents, how do they work, and name at least three: | Substances added to the testing system to increase the binding of antigens and antibodies. Examples are albumin, LISS, polybrene, PEG |
| What are Coombs Control Cells and what is their purpose? | RBCs coated with human IgG antibody that are added to a negative AHG tube to ensure proper function of the AHG reagent. |
| What does it mean if the Coombs Control Cells do not agglutinate? | AHG reagent was omitted or inactivated, or test system was not washed adequately to remove all protein. |
| Describe the purpose of the Autocontrol and what it means if it is positive: | Testing of the patient's serum or plasma with their own red blood cells to determine if autoantibody is present. If it is positive, the patient may have free autoantibody in their serum or plasma. (Usually DAT run next & positive) |
| What tests are performed on a patient's sample in order to administer units of packed RBCs? | ABO/Rh, Ab screen and crossmatch |
| If an antibody screen on a patient is negative, what is the chance that a crossmatch would be INCOMPATIBLE? | Less than 1% chance |
| How are enzymes helpful in antibody identification? | Enzymes destroy Duffy and MNS antigens. Enzymes also enhance some reactions (such as Rh) |
| What is the difference between a major and minor crossmatch, and which one do we routinely perform now? | Major Crossmatch is patient's serum or plasma with donor RBCs. Minor crossmatch is patient's RBCs with donor's plasma (not used any more) |
| What can be used to assist in clotting of a sample from a patient on anticoagulant therapy? | Thrombin or glass beads may be added to enhance clotting. If heparin is present, protamine sulfate may speed clotting. |
| What are the limitations to Compatibility Testing? What percent of antibodies are NOT detectable after 5 years? | Patient may have Ab present that is too low to detect (1/3 of alloAbs are not detected after 5 years) |
| What must be checked before issuing blood to a person from the Blood Bank? What must be checked before hanging a unit on a patient? | Recipient's name, ID |
| What is informed consent? | Physician or designee must educate patient as to risks involved in transfusions of blood and blood products, and must be signed by patient or representative prior to receipt of blood (unless severe emergency) |
| What is the Maximum Surgical Blood Order and how does it work? | Average number of units usually needed by patient for specific surgeries set up on all patients in advance. |
| What is elution and when is it used in the Blood bank? | Procedure to remove antibody from the RBC surface (coated in vivo). Acid, Heat, or Freeze are techniques used. |
| What is an adsorption and when is it used in the Blood Bank? | Procedure used to remove autoantibody form a patient's serum or plasma. Pull auto out of the patient's serum so that clinically significant alloAbs can be detected. Used in Warm Autoimmune Hemolytic Anemias (WAIHA) |
