Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
blood bank
| Question | Answer |
|---|---|
| IgG | Monomer, best reacts at body temp, coats but does not directly lyse RBCs, induced by pregnancy and transfusions, can cross the placenta |
| IgM | Pentamer, reacts best below body temp, binds complement and lyses RBCs, not induced by pregnancy, can cross placenta |
| LISS | Low Ionic Strength Saline: Decreases repulsive charges between RBC (zeta potential), allowing them to get closer together for greater antibody bridging |
| Draw back to using LISS | tends enhance expression of cold antibodies and autoantibodies |
| 22 % Albumin | Decreases zeta potential. Used less commonly than LISS |
| PEG | Polyethylene Glycol: Excludes H2O and allows RBCs to get closer during centrifugation. Generally greater sensitivity than LISS or albumin |
| Draw back to using PEG | Tends to enhance expression of warm antibodies and autoantibodies. May lead to false positive reactions at 37°C from nonspecific agglutination |
| Tube testing: Immediate Spin | Positives are usually IgM and insignificant if not ABO |
| Tube testing: 37°C | Add potentiator if desired and incubate at 37°C • LISS 10-15 minutes • Albumin 15-30 minutes • PEG 15 minutes DO NOT read at 37°C due to false positives • No potentiation/saline 30-60 minutes |
| Tube testing: Indirect antiglobulin test (IAT) | Wash to remove unbound globulins. Immediately add antihuman globulin (AHG). Check cells if needed. Antibodies reacting at IAT are more often significant |
| Antiglobulin test: Indirect | Demonstrates in-vitro (outside the body) RBC coating with antibody and or complement |
| Antiglobulin test: Direct (DAT) | Patient washed RBCs, then mixed with antihuman globulin; demonstrates in-vivo (within the body) RBC coated with antibody and or complement |
| Specific antiglobulin | • Anti-IgG-C3 Polyspecific, most commonly used. • Anti-IgG • Anti-C3-Cb |
| Dosage | Some antibodies react more strongly with RBC antigens that result from homozygous codominant gene expression resulting in “double-dose” antigen expression |
| Most common dosage | Kidd, Duffy, Rh, MNS |
| Enzymes | Proteolytic enzymes (ficin, papain) cleave RBC surface glycoproteins. This may destroy certain RBC antigens and may strengthen reactions by allowing antibodies to bind better to previously shielded antigens |
| Enzymes that destroy antigens | Duffy, MNS Mr. Duffy's MNS are destroyed |
| Enzymes that enhance antigens | I, Kidd, Lewis, Rh I had a Kidd named Lewis with an Rh problem |
| Neutralization | Certain substances when mixed with a red cell antibody, inhibit the activity of that antibody against test red cells • ABO- Saliva (secretor) • Lewis- Saliva (secretor for Leb) • P1- Hydatid cyst fluid and Pigeon egg whites |
| Lectins | Seed/plant extracts react with certain RBC antigens |
| A1 lectin | Dolichos biflorus |
| H lectin | Ulex europaeus |
| General characteristic blood group antigen | Protein, glycoprotein, or glycolipid on RBC |
| ABO system Type 1 chains | Glycoproteins in secretions and glycolipids in plasma carrying free-floating antigens |
| ABO system Type 2 chains | Glycolipid and glycoproteins bound to RBCs |
| ABO system Se (secretor) gene | Required to make A and B antigens in secretions • FUT enzyme adds fucose to type 1 chains at terminal galactose, product is type 1 H antigen • 80% gene frequency |
| H gene | FUT enzyme adds fucose to type 2 chains at terminal galactose, product is type 2 H antigen • Virtually 100% gene frequency (Bombay=hh) |
| H antigen is required before making what on the RBC | A and or B antigen on in secretions |
| Group A sugar | N-acetylgalactosmine |
| Group B sugar | Galactose |
| ABO antigens appear on fetal RBC at blank and reach adult levels at blank | 6 weeks gestation and reach adult levels by age 4 |
| ABO antibodies | Clinically significant naturally occurring that can causes sever acute hemolytic reactions and common but mild HDFN |
| Group O genotype | Genotype OO • Most common blood group across racial lines • Antigen: H • Antibodies: anti-A, anti-B, anti-A,B |
| Group A genotype | Genotype AA or AO • Antigen: A and H • Antibodies: anti-B (primarily IgM) |
| Group A subgroups | A1 (80%) and A2 (~20%) • A1 RBCs carry 5X more A antigen |
| Group B genotype | Genotype BB or BO • Antigen: B and H • Antibodies: anti-A (primarily IgM) • Subgroups usually unimportant |
| Group AB genotype | Genotype AB • Antigen: A and B very little H • Can be subdivided into A1B or A2B • Antibodies: NO ABO antibodies • Least frequent ABO blood type (4%) |
| ABO discrepancies: antigen problems (missing) | • A or B subgroups • Transfusion or transplant • Acute Myeloid Leukemia or other malignancies |
| ABO discrepancies: antigen problems (unexpected) | • Transfusion or transplantation • Acquired B phenotype • Bone marrow/stem cell transplant • Polyagglutination |
| ABO discrepancies: antibody problems (missing) | • Immunodeficiency • Neonates, elderly, immunocompromised • Transfusion or transplantation • ABO subgroups |
| ABO discrepancies: antibody problems (unexpected) | • Cold antibodies (auto or allo) • Anti-A1 • Rouleaux • Reagent related antibodies |
| Acquired B phenotype | A1 RBC contact with gram Neg; colon cancer, intestinal obstruction • Bacterial enzymes deacetylate group A GalNAc; what remains galactosamine looks like B and reacts with forms of monoclonal anti-B • AB front (with weak anti-B reactions), A back |
| B (A) phenotype | Opposite of acquired B (group B patients with weak A activity) this is inherited NOT acquired |
| Bombay (Oh) phenotype | Total lack of H, A and B antigens due to lack of H AND Se genes (genotype: hh, sese) • Naturally occurring strong anti-H, anti-A, and anti-B • O front type, O back type, but antibody screen wildly positive and all units incomp |
| Lewis system | • Type 1 chain only (glycoproteins in secretions, glycolipids in plasma) • Lea antigens cannot be modified to make Leb |
| Lewis secretors | Se enzyme adds fucose, then Le enzyme adds fucose: results = Leb |
| Lewis non-secretors | Lea is only possible Lewis antigen |
| Lewis antibodies | Naturally occurring, cold reacting IgM • Neutralize with saliva from secretors |
| Lewis consequences of incompatibility | • Antibodies are generally insignificant • Rare hemolytic transfusion reactions (more commonly seen with anti-Lea) • Minimal to no HDFN (antibody doesn’t cross placenta and Le antigens are not present on fetal RBCs) |
| Weird stuff about Lewis | • Lewis antigens decrease during pregnancy • Increased plasma volume dilutes antigen and increased plasma lipoproteins bind the antigens • Infection associations: H. pylori, Le(a-b-) risk for Candida and E. coli infection |
| I and i system | Antigens built on type 2 chains • Expression is age dependent • Simple chain on neonates = i • Branched chains in adults = I |
| I and i antibodies | Naturally occurring, common, usually insignificant cold reacting IgM |
| Auto-anti-I | Cold agglutinin disease also seen in Mycoplasma pneumonia infections |
| Auto-anti-i | Associated with infectious mononucleosis |
| P1 antigen | Naturally in pigeon/dove egg whites/feces and hydatid cyst fluid (Echinococcus) |
| Pk antigen | Most RBC adults have very little Pk (almost all converted to P) |
| P antigen | Very high frequency (99.9%) |
| Anti-P1 | • Most common • Cold reacting naturally occurring insignificant IgM • Can be neutralized |
| Auto-anti-P | • (Paroxysmal cold hemoglobinuria) • Biphasic IgG autoantibody with unique features binds in cold temps, hemolyzes when warmed to 37°C • seen following viral infection in children (syphilis historically) |
| R1 | DCe |
| R2 | DcE |
| R0 | Dce |
| Rz | DCE |
| r' | dCe |
| r'' | dcE |
| r | dce |
| ry | dCE |
| Rh system | 2nd most important blood group after ABO |
| Rh antibodies | Exposure requiring, warm-reacting IgG • D induces the most antibodies • HTR with extravascular hemolysis • Severe and prototypical HDFN |
| D negative phenotype | • Unusual because caused by mutations and deletions rather than by synthetic actions of a gene product • Whites: D-negatives have deletion of RHD gene • Blacks: point mutations in RHD gene (“pseudogene”) • Asians: usually have inactive RHD gene |
| D variants: Weak D | • Quantitative defect in D antigen (less D than normal) • Weak D requires IAT to detect D presence • Possible reason for weak D Point mutation causing altered amino acids C in trans position inhibits D |
| D variants: Partial D (D mosaic) | • Qualitative D antigen defect (abnormal forms, missing parts of the antigen) • Cause: RHD gene mutations leading to alteration of exterior part of RHD antigen • Antibodies form against absent parts of RHD • Classic: anti-D in a D-positive person |
| Why partial D vs Weak D matters | • Partial D moms NEED RhIg • Partial D recipients may make anti-D when receiving D pos RBCs |
| D variants: DEL | Appear D neg but have tiny amounts of D seen after elution of reagent anti-D from RBCs • Primarily seen in Asians |
| Anti-E commonly accompanied by blank | Anti-c but not necessarily vice-versa • Only way to get exposure to E is to also get exposure to c (R2 haplotype) |
| Rh null phenotype | Patients lack all Rh antigens |
| G antigen | Presents when either C or D is present • D neg mom has anti-G she NEEDS RhIg |
| Anti-G reacts againts | D+ C+ D-C+ D+ C+ |
| f antigen | Present when RHce is inherited (r and RO) • Often seen with anti-e or anti-c • Can cause mild HDFN and HTR |
| Kidd antigens | Jka, Jkb, Jk3 • Jka slightly more common than Jkb in blacks but similar in whites and Asians |
| Kidd antibodies | Exposure requiring, warm-reacting IgG (many with IgM component as well) • Can fix complement (IgM) • Sever acute HTR possible • Dosage effect • Variable antibody expression often disappears with time (<3 months) |
| Kidd transfusion reaction | Delayed HTR is most famous association • Intravascular and often sever • Mild HDFN at worst (child can only be single-dose antigen different from mom) |
| MNS antibodies | • Anti-M and anti-N are mostly opposite of anti-S and anti-s and anti-U • Usually ignored unless reactive at 37°C • Enzymes generally decrease all MNS antigens except U |
| N-like antigen | Not true N antigen but close enough to prevent most M+N- from making anti-N • Anti-N nearly excusive to blacks |
| Auto-anti-N | Induced by hemodialysis • Formaldehyde sterilization of machine • Modification of N lead to rare autoantibody |
| Duff antigens | • Fya high frequency in Asians • Fyb high frequency in whites • Fy(a-b-) most common in blacks |
| Fy(a-b-) | Due to inheritance of 2 copies of Fy gene which gives no function Duffy glycoprotein • Fy ias an Fyb variant that doesn't make Fyb antigen on RBC BUT does in non-RBC body tissues |
| Duffy antibodies | • Anti-Fya more common and significant than anti-Fyb • Exposure requiring, warm-reacting IgG • Marked dosage and variable expression |
| Consequences of incompatible Duffy | Sever HTR, usually delayed and extravascular • Often mild HDFN |
| Fy(a-b-) is resistance to what infections | Malaria (Plasmodium vivax) |
| Kell antigens | • Low frequency: K, Jsa, Kpa • High frequency k, Jsb, Kpb, Km |
| Kell antigens are destroyed by blank but not by blank alone | Destroyed by thiol reagent but not by enzyme alone • DTT reagent break the disulfide bonds |
| Anti-K | • Most common non-ABO antibody after anti-D • Exposure requiring, warm-reacting IgG • Most common from transfusion than pregnancy |
| Anti-k | • Very uncommon due to high antigen frequency • Exposure requiring, warm-reacting IgG • More common from transfusion than pregnancy |
| Consequences of incompatible Kell | • Sever HTR, may cause acute or delayed, usually extravascular • Sever HDFN, less common, damages early RBC precursors so it may be suppressive as well as hemolytic • Significant at low titers (1:8 =critical) |
| Lutheran antigens | • Lua =low frequency 5-8% • Lub =high frequency 99% |
| Lutheran antibodies | • Uncommon • May be naturally occurring (anti-Lua) • Not usually significant |
| Vel system | • Extremely high frequency >99% in all populations • Antibodies is a mix of IgG and IgM • May cause sever HTR and HDFN • May interfere with ABO typing due to reaction at room temp |
| HTLA antibodies (High Titer Low Avidity | • High frequency antigens that are generally clinically benign (no HDFN) |
| When should a transfusion reaction workup be done | Indicated when possible reaction is suspected by combination of Inflammatory, Circulatory, Pulmonary, Coagulation, Psychological |
| Transfusion reaction workup (blood bank testing) | • Clerical check • Visible hemoglobinemia in post transfusion sample • DAT test • Repeat ABO Rh • Repeat antibody screen, XM • Elution |
| Non-blood bank test for transfusion reaction workup | • Haptoglobin • Direct and indirect bilirubin • LDH (Lactate dehydrogenase) • Urine hemoglobin |
| Classifications of transfusion reactions presenting with fever | • Acute: acute hemolytic, febrile non-hemolytic, transfusion-related sepsis, TRALI • Delayed: delayed hemolytic, TA-GVHD |
| Classifications of transfusion reactions presenting without fever | • Acute: allergic, hypotensive, Tx-associated dyspnea, TACO • Delayed: delayed serologic, post-transfusion purpura, iron overload |
| Acute hemolytic transfusion reaction | Acute, presenting with fever • Clerical errors are most common cause • RBC destruction may be intravascular or extravascular • ABO related, intravascular usually more severe |
| Signs and symptoms of Acute hemolytic transfusion reaction | • Fever and chills is the most common • Back pain or infusion site pain • Hypotension/shock • Hemoglobinuria • DIC/increase bleeding • Sense of impending doom |
| Lab findings of Acute hemolytic transfusion reaction | • Hemoglobinemia (pink/red plasma/serum) can last sever hours • Hemoglobinuria (usually clears be end of the day) • Positive DAT (unless donor cells destroyed) may be mixed field • Elevated in/direct bilirubin • RBC abnormalities • Coaga |
| Febrile non-hemolytic transfusion reactions | Acute, presenting with fever • Historically most frequently reported reaction now <1% due to leukoreduction • Unexplained increase of temp by 1°C or 2°F • Causes: increased pyrogenic substances mostly from WBCs |
| Signs and symptoms of Febrile non-hemolytic transfusion reactions | • Transient fever/chills during or up to 2hrs post transfusion • Symptoms usually later in transfusion (esp. Plts) • Chills may be first, fever may be delayed up to 1hr+ after transfusion • Premedicated or head injury patients may never have fever |
| Lab findings of Febrile non-hemolytic transfusion reactions | There are non |
| Transfusion related sepsis | Acute, presenting with fever • Plts are contaminated by skin by collection process • RBC are more often contaminated by an organism growing in the donor's blood (often asymptomatic) • Gram neg that like cold temps • Gram pos less common |
| Signs and symptoms of Transfusion related sepsis | • Earlier symptoms seen in more severe reactions and more often with RBC transfusions • Rapid onset high fever (often >4°F/2°C) • Rigors (true shaking chills with rigidity) • Abdominal cramping, nausea/vomiting • Hypotension/shock • DIC |
| Lab finings in Transfusion related sepsis | • Discolored RBC product (+/-) contaminated RBCs may turn DARK or purple • May have Hemoglobinemia/uria (non-immune) • DAT negative (unless coincidental) • Gram stain + |
| Transfusion Related Acute Lung Injury (TRALI) | Acute, presenting with fever • #1 cause of transfusion related fatality in the US • New acute lung injury ≤6hrs post transfusion |
| Signs and symptoms of Transfusion Related Acute Lung Injury (TRALI) | •Usually fever • Chills • Transient hypertension than hypotension |
| Two event pathway TRALI | • 1st Pre-existing condition, activates lung endothelia cells and primes PMNs • 2nd transfusion of stored blood product (with or without donor antibodies) Stored blood accumulates BRMs-biologic response modifiers |
| Allergic reactions: mild transfusion reaction | Acute reactions presenting without fever • Mild allergic (urticarial, cutaneous) reactions • Very commonly reported reaction 1-3% • Localized hives, +/- more severe swelling around eyes and lips (angioedema), mild respiratory |
| Allergic reactions: moderate transfusion reaction | • Some reactions fall between the 2 extremes • May present with upper/lower airway obstruction +/- cutaneous manifestations • Upper: hoarseness, lump in throat • Lowe: wheezing, chest tightness, dyspnea |
| Allergic reactions: severe transfusion reaction | • Anaphylactic reactions • Uncommon • Anaphylaxis very early in the transfusions • Acute hypotension, lower airway obstruction, abdominal distress, systemic crash • Most patients have skin findings (urticaria, generalized pruritus itching) |
| What is the allergen in allergic reaction | • Classic: IgA deficient recipient with IgG anti-IgA • Latex, drugs, food in donors can lead to severe reactions in susceptible recipients (rare) |
| Prevention of Allergic reactions transfusion reaction | • Washed cellular products for those with severe reactions and no demonstrable IgA deficiency • Benadryl insufficient by itself may use corticosteroids +/- additional histamine blockers |
| Acute hypotensive reactions transfusion reaction | Acute reactions presenting without fever • Reactions similar to severe allergic reactions but no skin symptoms • >30mmHg drop in systolic BP, diastolic ≥80 • Occurs <15mins after stat of transfusion • Resolves <10mins after transfusion stopped |
| Transfusion associated dyspnea (TAD) | Acute reactions presenting without fever • Acute respiratory distress <24hrs after transfusion • TRALI, TACO, and allergy ruled out |
| Transfusion associated circulatory overload (TACO) | Acute reactions presenting without fever • Acute onset of congestive heart failure as a direct result of blood transfusion |
| Signs and symptoms of Transfusion associated circulatory overload (TACO) | • Dyspnea, orthopnea, bilateral rales, with hypoxia • Systolic hypertension (widened pulse pressure), tachycardia, JVD, pedal edema, headache • Usually afebrile • X-ray with bilateral basilar infiltrates, widened cardiac silhouette |
| Who is at risk for Transfusion associated circulatory overload (TACO) | • Patients with pre-existing CHF • Very old (>85% occur in patients >60) and very young (to a lesser extent) • Renal failure • Chronic anemias due to compensation for anemia with increased plasma volume • ANY patient getting rapidly transfused |
| Delayed hemolytic transfusion reactions (DHTR) | Delayed reactions presenting with fever • Hemolysis at least 24hrs but less than 28 days after transfusion • Pt exposed to non-self RBC, antibody form and fades, pt re-exposed and rapid production of IgG antibody •Typical for Kidd, Duffy, Kell |
| Signs and symptoms of Delayed hemolytic transfusion reactions (DHTR) | • Often completely asymptomatic • Fever and anemia of unknown origin • Mild jaundice/scleral icterus may be seen |
| Lab findings of Delayed hemolytic transfusion reactions (DHTR) | • Icteric serum • DAT positive (classically “mixed field”) • Anemia • Newly identified RBC antibody • Spherocytes on peripheral smear • Elevated LDH and indirect bilirubin, decreased haptoglobin (even if extravascular) |
| Transfusion associated graft Vs. host disease (TA-GVHD) | Delayed reactions presenting with fever • Results from an attack on recipient cells by viable T-lymphocytes in a transfused blood product |
| Delayed Serologic Transfusion Reaction (DSTR) | Delayed reactions presenting without fever |
| Post-transfusion Purpura (PTP) | Delayed reactions presenting without fever • Rare, with marked thrombocytopenia and increased risk of bleeding about 10 days following transfusing (may be below 10,00/uL) |
| Iron overload transfusion reaction | Delayed reactions presenting without fever |
| Warm autoantibody | • Most are IgG • DAT positive with anti-IgG alone or with anti-C3d • Eluate reacts with all RBCs • Due to broad specificity all cross matches usually incompatible • May have to do absorption • May have to give least incompatible |
| Cold autoantibody | • 2 main categories: Cold agglutinin disease/syndrome (CAD) and paroxysmal cold hemoglobinuria (PCH) • Typical: IgM reacting best at 4°C • DAT positive with complement only • Antibodies causing hemolysis also react at 37°C • May need to prewarm |
| Mixed-type autoimmune hemolytic anemia | • Very common • Both IgM to react in cold and IgG to react at body temp • DAT positive with both anti-IgG and anti-C3d • Typically present with severe hemolysis • Treat like WARM |
| Drug-related autoimmune hemolytic anemia | • Wide variety of drugs can cause antibody formation and variable levels of hemolysis •First drug adsorption to membrane, immune complex formation, and autoantibody induction |
| Sickle cell disease | Common in American Americans with hemoglobin S mutation leading to RBC deformity |
| Neonatal transfusions (birth-4months) | Need Leukocyte reduction, Irradiation, CMV neg, and HbS neg |
| Hemolytic disease of the fetus/newborn (HDFN) | • ABO HDFN is most common |
| Lab test for Hemolytic disease of the fetus/newborn (HDFN) | • Cord blood DAT +/- • Antibody screen • Elution • Indirect bilirubin elevated |
| 1 vial of RhIg = how many ml | 30ml |
| Formula to calculate how many vials of RhIg | KB% X 5/3 = number of vials |
| Whole blood donation is every | 8 weeks |
| Double red donation is every | 16 weeks |
| Single platelet apheresis is every | 2 days |
| Permanent donor deferral | • Infection risk • HIV • Receiving money or drugs for sex • Serologic positive for HIV, HBV, HCV, HTLV • Transfusion of clotting factor concentrates (in hemophilia) • History of Babesiosis or Chagas’ disease |
| 3 year donor deferral | • Infectious risk • Recovered from malaria • Immigrants from malaria-endemic countries (after living there for 5 years consecutive) |
| 1 year donor deferral | • Needle sticks or other contact with blood • Sex with person with HIV, hep, who used needles for drugs • Rape victims • Incarcerated >72hrs consecutive • Transfusions • Tattoos/piercings • Travel to malaria-endemic areas • Syphilis/gonorrhea |
| Pregnant women donor deferral for | 6 weeks postpartum |
| Fresh Frozen Plasma (FFP) | (Rh matching is not necessary for plasma) • -18C or colder • Expires 1 year after freezing • Once thawed expires within 24 hours • MUST be ABO compatible • Used for factor XI deficiency |
| Cryoprecipitate | (Rh matching is not necessary for plasma) • -18C or colder • Cold insoluble portion of FFP (FFP-frozen, thawed, spun) • Transfuse within 6 hours after thawing • Used for Factor XIII and fibrinogen deficiencies and Hemophilia A |
| Packed RBC | • 1-10C • Hct 80% • Expires weeks from draw date |
| Frozen RBC | • -65C or colder • 80% of original RBC and <1% of glycerol • Frozen expires 10 years and once thawed and deglycerolized 24 hours |
| Platelets | • Try to give Rh matching otherwise give RhIg • 20-24C (room temp) while continuously rotating • Expires depending on the type of bag, average 5-7 days • QC: pH >6.2 and 5.5X10^10 plt/unit • Infants transfuse ABO compatible |
| Irradiated blood | • Prevents graft VS host disease (GVHD) • Recommended for immunosuppressed/immunocompromised patients including IUT, recipients of units from blood relative and recipients who have undergone bone marrow transplant |
| What component of choice for a patient in DIC with a low fibrinogen level? | Cryoprecipitate is used because of the high concentration of fibrinogen. (FFP can be used to restore the depleted coagulation factors) |
| ABO discrepancies with Red cells: Rouleaux | • Failure to wash. • Repeat with Saline washed cells |
| ABO discrepancies with Red cells: Mixture of cell types | Check transfusion hx |
| ABO discrepancies with Red cells: Subgroups (A2) | Test with anti-A1 for A subgroups |
| ABO discrepancies with Red cells: Disease processes (acquired B) | Check pt diagnosis, Leukemia or bacteria-acquired B |
| ABO discrepancies with plasma/serum: Rouleaux | • Due to increased protein (Multiple Myeloma or Waldenstrom’s) • Saline replacement |
| ABO discrepancies with plasma/serum: Room temp or cold reacting antibody | • Mini cold screen • Age- elderly antibody production decreased and newborn antibody has not reached optimum levels |
| Rh immune globulin (RhIg) given when to pregnant females | At 28 weeks and within 72hrs of delivery |
| HLA system (Human Leukocyte Antigens) | • Polymorphic system of antigens present on all nucleated cells (also small amount of HLA antigen on red cells) • Genes located on short arm of chromosome 6 (major histocompatibility complex) • Extremely useful in paternity testing |
Created by:
evk2369
Popular Laboratory Science sets