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Blood Bank Beautiful
Blood Bank for the Beautifuls
| Question | Answer |
|---|---|
| Used to render donor lymphocytes non-functional and protects against graft-versus- host disease in bone marrow transplant recipients, directed donations, immuno-suppressed patients | Irradiators |
| Red cells expire 28 days after they are irradiated | gamma irradiation |
| Standard refrigerators maintained at 1 to 6C for storage of ??? | RBC and whole blood |
| Freezers maintained at -18C or lower for ??? | FFP and Cryoprecipitate |
| Freezers maintained at -65C or lower for ??? | frozen RBC |
| Use to prevent the formation of platelet aggregates and optimize the exchange of gases required for platelet survival. Gentle rocking motion at room temperature | Platelet rotators |
| Request and Issue of blood products? Name them | Red blood cells FFP platelets cryoprecipitate granulocytes coagulation factors albumin |
| Some tests done in reference lab | Resolving ABO/Rh discrepancies Antibody identification Warm and cold auto-antibodies Transfusion reaction Investigation of positive DAT |
| Gel technology eliminated the need for multiple washes with saline and for control cells. T/F? | T |
| all non-secretors of ABH antigen were Le(a+) | |
| Lewis antigens are produced by tissue cells and secreted into body fluids (primarily secretions and plasma )then adsorbed onto the red cell membrane. They ARE NOT intrinsic to RBCs | |
| Le(a-b-) in newborns | |
| By age 6 to 7 the child’s true Lewis phenotype can be established. | |
| Lewis antigens previously present on a woman’s red cells may disappear while she is pregnant resulting in Le(a-b-) phenotype | |
| The two most common antigens are: P1 and P2 P1 is poorly developed on the red cells of new born and develops to full strength at about 7 years. The P1 antigen deteriorates rapidly on storage at 4C | |
| IgM Reactive in saline 4C – 22C | Anti-P1 |
| IgM and IgG; react over a wide thermal range Bind complement efficiently; potent hemolysins Potential to cause severe hemolytic transfusion reactions and HDN Associated with increased incidence of spontaneous abortions in early pregnancy | Anti-PP1Pk |
| paroxysmal cold hemoglobinuria(PCH) IgG Biphasic hemolysin Binds to P-positive red cells at lower temperature in the extremities Complement is activated Red cells lyse when warmed to 37C Demonstrated by the Donald-Landsteiner Test | Autoanti-P |
| Cysts of Echinococcus granulosus Extracts of liver flukes, earthworms and roundworms Roe from salmon and trout Pigeon egg white -can be used for neutralization | Sources of P1 |
| Allo-anti-I Rare, only seen in adult “i” phenotyped patients Maybe IgM or IgG Do not react with autologous cells Transfused with compatible adult “i” blood | |
| Auto-anti-I Common autoantibody that can be found in virtually all sera when testing is done at room temperature or below. The antibody is almost exclusively IgM Titer less than 64 at 4C | |
| Pathogenic autoanti-I Transient anti-I found in the serum of patients with atypical pneumonia due to Mycoplasma pneumoniae or some parasitic infections. This antibody rarely causes red cell destruction | |
| Pathogenic autoanti-I Cold hemagglutinin disease – antibody may attach to red cells and bind complement at low temperatures in the peripheral circulation, when body warms intravascular hemolysis occurs when blood is re-warmed in the body core | |
| Alloanti-i No examples have been discovered | |
| Auto- anti-i Mostly IgM, React best in saline at 4C Gives strong reactions with cord RBCs and adult “i” RBCs and weaker reaction with adult I RBCs. Seen in patients with Infectious mononucleosis( Epstein –Barr virus), Has been associated with HDFN | |
| Membrane of leukocytes and platelets In plasma and serum Saliva, human milk, colostrum, amniotic fluid, Urine, hydatid cyst fluid | Other sources of I and i antigen |
| Unlike ABO system absence of Rh antigens does not typically correspond with the presence of antibody in the plasma/serum Production of Rh antibodies requires immune red blood cell stimulation: Transfusion, pregnancy | |
| Most individuals who are C+ are Cw+ Antibodies to these antigens can be naturally occuring and may play a role in HFDN and HTR | |
| Order of immunogenicity: D > c > E > C > e Do not bind complement, extravascular destruction. | |
| K antigens sensitive to treatment with sulfhydryl reagents – they reduce the disulfide bonds creating red cells that lack Kell antigens | |
| McLeod Syndrome Associated with chronic granulomatous disease | k, Kpb and Jsb |
| Duffy antibodies frequently delayed | |
| Anti-K excluded using 2 single dose antigen positive cells. Anti-P1 excluded using 3 antigen positive cells. Anti-f, -V and -Xga excluded using 1 antigen positive cell. A single dose expression acceptable: Cw, Lua, Kpa, and Jsa. Exclude if hetero. | Antibody Exclusions |
| Determined that Fya and Fyb served as receptors or attachments for invasion of cells by malarial parasites. The absence of these receptors conferred the resistance to malaria seen in Fy(a-b-) blacks. | |
| Cause HDN and delayed hemolytic transfusion reactions Deteriorate rapidly in vivo and in vitro Level of antibody may decrease where it is no longer detected by serological testing | Kidd |
| Characteristic mixed field agglutination | Lutheran |
| Rare antibody due to the antigen’s high incidence IgG Clinically significant. Usually produced following transfusion or pregnancy. Most examples of anti- Lub agglutinate in antiglobulin phases Some demonstrate mixed field agglutination | Anti- Lub |
| Xga antibodies Anti- Xga is uncommon. Usually IgG. Binds complement without in vitro hemolysis. Destroyed by enzymes Does not cause HDN or HTR | |
| Sda antibodies Naturally occurring IgM Not considered clinically significant Have a characteristic reaction that is mixed field of small tightly agglutinated, refractile clumps with a background of free flowing cells | Sda antibodies |
| Phenotyping the patient’s RBC DAT test Selected Cells Neutralization Chemical treatment: Proteolytic enzymes Sulfhydryl reagents ZZAP | Several procedures can be performed to identify multiple antibodies |
| People don’t make alloantibody to antigens they possess. Test patient’s red cells for the corresponding antigen. Negative result confirms the identified antibody. Positive results=antibody being incorrectly identified or there is a false-positive | Phenotyping the Patient |
| If positive due to IgG coating the cells the IAT may give false positive results.The antibody coating the cells blocks the antigen sites preventing the typing serum from reacting.AHG reacts with the coating antibody giving a false positive reaction. | Positive (DAT) Need to perform an elution – removes the antibody coating the cells, to get an accurate phenotype.If antibody resists the elution technique then absorption method is used |
| Inactivated: Duffy, MNSs, Xga Enhanced: ABO, Rh, Kidd, Lewis, I, P1 | Enzymes |
| Cleave the disulfide bonds of IgM molecules and help differentiate between IgM and IgG antibodies Dithiothreitol (DTT) is a thiol and will denature Kell antigens 2-mercaptoethanol (2-ME) | Sulfhydryl Reagents |
| A combination of proteolytic enzymes and DTT Denatures Kell, M, N, S, Duffy Good for adsorption techniques “frees” autoantibody off patient’s cell, so that autoantibody can then be adsorbed onto another RBC | ZZAP |
| Adsorption procedures used to investigate underlying alloantibodies. ZZAP/chloroquine diphosphate dissociate IgG antibodies from the RBC. After patient RBCs incubated, the adsorbed serum is tested with panel cells to ID the alloantibody (if present) | Adsorption |
| Uses known red cells either match the patient’s phenotype or have antigens that selectively remove certain known antibody specificities | Alloantibody/Differential Adsorption |
| Twofold serial dilution performed against target red cells Titer level is the reciprocal value of the greatest dilution where agglutination is observed. | Antibody Titration |
| Comparison of current and original testing results indicates if a significant change has occurred – fourfold increase | Antibody Titration |
| Plt count for random donors =5.5 x 1010/L Plt count for apheresis donors=3.0 x 1011/L pH >6.2 | QC Platelet |
| Generally transfusion is given when platelet count is below 20 x 10⁹/L | Platelet Therapy |
| Not usually indicated for patients with - ITP- idiopathic thrombopenic purpura (↑destruction) -TTP–thrombotic thrombocytopenic purpura - DIC- (↑ consumption) - HUS-hemolytic uremic syndrome | Platelet Therapy |
| 1 unit of platelet raises adult count by 5 x 10⁹/L when measured 10 mins to 1 hour after completion. The rate of increase is usually higher if apheresis platelet are given 8-10 x 10⁹ /L | Platelet Therapy |
| It is frozen within eight hours of collection | FFP |
| Plasma is stored frozen by the manufacturer at temperatures < -180C for up to 12 months or < -65 0C for 7 years | |
| A single unit of FFP or FP24 from whole blood collection should contain 150 to 250 mL of plasma. | |
| Used to treat replacement of multiple clotting factors in patients with liver disease, DIC, vitamin K deficiency, warfarin overdose, or massive transfusion. | FFP and FP24 |
| Useful for treatment of warfarin overdose or reversal or factor X1 deficiency. Use for plasma exchange for TTP, HUS or HELLP patients | Thawed and Liquid Plasma |
| Requires 45 min. to thaw a double bag Requires 30 min. to thaw a single bag Plasma should be thawed in a 37 0C water bath. Thawed FFP and FP24 has an expiry date of 24 hours. Thawed cryo-free supernatant has an expiry date of 72 hours | Preparation of Frozen Plasmas |
| Thawed cryo-free supernatant has an expiry date of 72 hours | |
| Plasma (FFP) should be transfused immediately after release from the Blood Bank because Factor V and VII will deteriorate rapidly at room temperature | |
| Used to replace four specific factor deficiencies: Factor VIII, von Willebrand Factor, fibrinogen, and fibrinonectin, Factor XIII. | Cryo Therapy |
| The replacement of one or more blood volumes, or about 10 units (adults) within 24 hours | Massive Transfusion |
| Blood units less than 7 days old are preferred to reduce the risk of hyperkalemia and to maximize the 2,3-diphosphoglycerate levels | Neonatal Transfusion |
| Primary immunodeficiencies Secondary hypogammaglobulinemia CLL, post bone marrow transplant recipients Immune thrombocytopenic purpura (ITP) Kawasaki syndrome Guillain-Barré syndrome | IVIG |
| Hemoglobinemia( plasma pink or red) Hemoglobinuria( urine pink, red, brown or almost black) Decreased serum haptoglobin Elevated LDH | Lab Indicators of Intravascular Hemolysis |
| Increased serum bilirubin Spherocytes and agglutination Increased reticulocytes Decreased hemoglobin and hematocrit | Lab Indicators of Extravascular Hemolysis |
| Benign react with adult not cord Pathological react with both adult and cord cells | Pathologic Cold Autoagglutinins Anti-I and i |
Created by:
mastergogo
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