Free ASCP MLS Exam Blood Banking Mock Test – Part 65: Quality Assurance and Modern Practices

• In maternal antibody monitoring, a titer of 1:32 or higher is generally considered critical for most clinically significant antibodies (like anti-D, anti-K).

• This indicates a high risk of hemolytic disease of the fetus and newborn (HDFN) and warrants closer fetal surveillance, such as:

  • Middle cerebral artery Doppler

  • Possible early intervention or intrauterine transfusion

Other options are incorrect because:

• b) Normal immune response: Titers below critical levels are considered less risky.

• c) Low risk: 1:32 or higher is not low risk.

• d) False positive: Not applicable; titer reflects true antibody concentration.

• Weak D is caused by quantitative reductions in D antigen expression, often due to missense mutations in the RHD gene that reduce surface expression but preserve the D epitopes.

• Partial D is caused by qualitative changes in the D antigen, where part of the D protein is altered or replaced, also due to mutations in the RHD gene (often involving exons that encode external epitopes).

• Molecular assays for distinguishing weak D from partial D involve sequencing or targeted analysis of the RHD gene to identify the specific mutation.

• RHCE (b) relates to C/c and E/e antigens, not D.

• LW (c) and RHAG (d) are unrelated to D variant typing.

• For blood bank storage equipment (like refrigerators, freezers) without continuous monitoring, standards (e.g., AABB, FDA) typically require manual temperature checks at least once every day.

• Some guidelines may require recording twice daily (morning and afternoon) for certain critical storage, but the most common and standard minimal requirement in blood banking for ambient temperature monitoring without automated systems is once daily.

• Given the options and typical exam context, once a day is the standard correct choice for ambient temperature monitoring in such cases.

• RhIG is given to prevent maternal sensitization to Rh(D) antigen.

• If both the mother and the baby are Rh-negative, there is no risk of exposure to D-positive red cells, so RhIG is unnecessary.

Other options are incorrect because:

• b) Mother is O positive: RhIG is not indicated based on ABO type; the mother’s Rh status matters.

• c) Preterm baby: RhIG may still be needed depending on gestation and exposure.

• d) Maternal infection: Infection does not negate the need for RhIG if there’s Rh incompatibility.

• Leukocyte-reduced red blood cells are processed to remove white blood cells while retaining the majority of RBCs.

• AABB Standards require that at least 85% of the original red cells be retained after leukoreduction.

• This ensures the unit remains therapeutically effective for transfusion while minimizing risks of:

  • Febrile non-hemolytic transfusion reactions

  • Alloimmunization

  • CMV transmission

Other options:

• 50% or 70% → insufficient RBC content.

• 100% → unrealistic, as some RBC loss occurs during filtration.

• Anti-E was identified in the panel at the antiglobulin phase — meaning AHG (Coombs) reagent caused agglutination in some cells.

• Check cells (IgG-sensitized red cells) were added to nonreactive tubes, but no agglutination was seen.

• Check cells should cause agglutination if the AHG reagent is working and was added properly — no agglutination means the negative AHG result is invalid.

• Therefore, the panel results are invalid because the negative reactions can’t be trusted (possible AHG reagent not added, or reagent problem, or wash failure).

• The proper action is to QC the AHG reagent and check cells and repeat the panel.

• Pretransfusion testing requires absolute certainty of patient identity.

• In this case:

  • Name, medical record number, and date of birth all differ between the sample and request.

  • Any discrepancy is considered unacceptable—it cannot be resolved by relabeling or adjusting the request.

• The only safe action is to:

  1. Obtain a new blood sample from the correctly identified patient.

  2. Submit a new transfusion request that exactly matches the patient’s identification.

• The Indirect Antiglobulin Test (IAT), also called the indirect Coombs test, is used to detect maternal antibodies present in serum that are not yet bound to red cells.

• In the context of HDFN, it identifies maternal IgG alloantibodies (e.g., anti-D, anti-K) that could cross the placenta and attack fetal red cells.

Other options are incorrect because:

• b) Fetal red cell antigens are not directly detected by IAT.

• c & d) Bilirubin and hemoglobin measurements require biochemical assays, not IAT.

• When preparing an eluate (removing antibody from sensitized red cells), the last wash of the RBCs is tested to ensure no free antibody remains.

• A nonreactive result confirms that all antibody has been removed and that any subsequent reactivity in the eluate is due to antibodies actually eluted from the patient’s cells, not residual plasma.

• Reactive washes (a) indicate incomplete washing and could cause false-positive results.

• The eluate’s reactivity relative to the DAT (c, d) is irrelevant for the wash control—it only applies to the final eluate testing.

Pathogen reduction technologies (such as amotosalen + UVA, riboflavin + UV, or methylene blue + light) work by cross-linking nucleic acids (DNA/RNA), which prevents pathogens (viruses, bacteria, parasites) from replicating.

• a) False — it does not promote antibody formation to microbial antigens; it inactivates pathogens.

• c) False — infectious disease testing is still required; pathogen reduction is an added safety measure, not a replacement for testing.

• d) False — DTT is not used in pathogen reduction; DTT is used in serology to disrupt IgM antibodies.

• Warm autoimmune hemolytic anemia (AIHA) often causes a positive DAT, coating the patient’s red cells with autoantibodies.

• Serologic typing can be unreliable because the patient’s RBC antigens may be masked or altered by the bound autoantibody.

• DNA-based testing (genotyping) evaluates the patient’s underlying blood group genes, allowing accurate determination of antigen profile without interference from autoantibodies.

Why not the others:

• a) HDFN: Antibody identification is done serologically, not genotypically.

• b) TRALI: Diagnosis is based on clinical criteria and donor antibody testing, not patient genotyping.

• c) Extracorporeal photopheresis: This treatment doesn’t affect antigen typing significantly, so genotyping is rarely needed.

• Kernicterus is a type of bilirubin-induced neurological damage in newborns.

• The most common cause is high levels of unconjugated (indirect) bilirubin that cross the immature blood–brain barrier.

• This can occur due to severe hemolysis, often from Rh-mediated HDFN, or less commonly from ABO incompatibility or other hemolytic conditions.

Other options are incorrect because:

• b) Maternal infection: May contribute indirectly but is not the primary cause.

• c) ABO incompatibility: Usually causes milder hyperbilirubinemia; severe kernicterus is less common.

• d) Iron deficiency: Does not cause kernicterus.

The computer (electronic) crossmatch relies on:

1. Confirmation that the patient has no clinically significant alloantibodies (current and historical).

2. ABO/Rh confirmation of both donor unit and patient.

3. Validated computer system to detect ABO incompatibility.

• a) Historical ABO/Rh alone is not enough — current sample must confirm ABO and rule out antibodies.

• b) The system must be validated for this use, but the key requirement is absence of clinically significant antibodies.

• d) Immediate spin crossmatch is not required for electronic crossmatch; it replaces the IS phase.

• In cases of suspected HDFN, bilirubin levels in amniotic fluid are measured using a spectrophotometric scan at 450 nm.

• This wavelength corresponds to the absorption peak of bilirubin, allowing quantification.

• The results are then interpreted using the Liley graph to assess the severity of fetal hemolysis.

Other options are incorrect because:

• b) Coombs test: Detects antibodies on red cells, not bilirubin.

• c) ELISA: Used for antigen or antibody detection, not routine bilirubin measurement.

• d) IAT: Detects unbound maternal antibodies, not bilirubin.

According to AABB Standards, apheresis granulocyte collections must contain ≥ 1.0 × 10¹⁰ granulocytes in at least 75% of units tested.

This ensures a sufficient therapeutic dose for effective treatment in patients with severe neutropenia and infections.

• The fetal screen (rosette test) is a qualitative test used to detect fetal Rh(D)-positive red cells in the maternal circulation.

• It helps determine whether an additional dose of RhIG is needed after events like:

  • Delivery

  • Miscarriage

  • Trauma

  • Invasive procedures

Other options are incorrect because:

• b) Maternal antibodies are detected by indirect Coombs (IAT).

• c) Bilirubin is measured by biochemical methods.

• d) Antibody titer is quantified by serial dilution, not rosette testing.

• Sterile connection devices (like welding devices used in blood banks or cell therapy) must be verified every time a weld is made to ensure the integrity of the connection.

• Quality control with each weld prevents contamination or leaks, which could compromise sterility.

• Periodic or daily checks alone are not sufficient because a single weld failure can occur at any time.

• A new lot of anti-B must react with B-positive cells and not react with B-negative cells.

• In this case, it fails both criteria (no reaction with B-positive and false reaction with B-negative), which indicates a serious problem with the reagent.

• Using it could lead to incorrect blood typing, which is a major patient safety risk.

• Proper procedure: do not use the lot, label it as “not for use,” and investigate (e.g., contact the manufacturer, check storage conditions, etc.).

• In Rh-mediated HDFN, maternal IgG antibodies cross the placenta and bind to fetal Rh-positive red cells, causing hemolysis.

• The breakdown of red cells releases hemoglobin, which is metabolized to bilirubin.

• This leads to hyperbilirubinemia in the fetus or newborn, which can cause jaundice or, in severe cases, kernicterus.

Other options are incorrect because:

• b) Reduced liver enzymes: Not a cause; liver may be immature but hemolysis is primary.

• c) Maternal iron deficiency: Does not directly cause fetal hyperbilirubinemia.

• d) Dehydration: Not the cause of increased bilirubin in HDFN.

• Proper patient identification requires a wrist or ankle band that is physically on the patient and includes:

  • Patient full name

  • Hospital/medical record number or ID

• This band must be verifiable at the bedside before blood collection or transfusion.

Why the others are not acceptable:

• b) Addressograph on bed → not on patient, can be swapped or misread.

• c) Verbal confirmation alone → insufficient; patient may be confused or unconscious.

• d) Chart with unattached armband → band is not on patient; identity cannot be confirmed.

• The Kleihauer–Betke test is an acid elution method that distinguishes fetal hemoglobin (HbF) from adult hemoglobin (HbA) in a blood smear.

• It is used to detect and quantify fetal red blood cells in the maternal circulation, which is important for determining the dose of Rh immune globulin needed after delivery or a sensitizing event.

• The other options:

  • b) Coombs test — detects antibody-coated red cells.

  • c) RPR test — screens for syphilis.

  • d) Hematocrit test — measures the percentage of red blood cells in blood.

• In ABO hemolytic disease of the fetus and newborn (HDFN):

  • Most commonly occurs when the mother is blood group O.

  • She produces IgG antibodies against A or B antigens on fetal red cells (since IgG can cross the placenta).

• Mothers with group A or B usually produce mostly IgM antibodies, which cannot cross the placenta, so HDFN is uncommon in these cases.

Other options are incorrect because:

• b & d) IgM antibodies cannot cross the placenta.

• c) Anti-H is not a common cause of ABO HDFN.

• The standard dose of Rh immune globulin (RhIG) is calculated to protect an Rh-negative mother from sensitization to up to 15 mL of fetal red blood cells, which is roughly equivalent to 30 mL of whole blood.

• If a larger fetomaternal hemorrhage occurs, additional doses of RhIG are given based on the volume of fetal cells detected (often using the Kleihauer–Betke test).

Other options are incorrect because:

• b, c, d) Do not match the standard protective volume used for routine prophylaxis.

• In Rh incompatibility, an Rh-negative mother carrying an Rh-positive fetus is usually not affected during the first pregnancy because she has not yet been sensitized.

• Sensitization typically occurs during delivery, miscarriage, abortion, or invasive procedures, when fetal red cells enter the maternal circulation.

• Subsequent pregnancies with an Rh-positive fetus are at risk for HDFN due to maternal anti-D antibodies.

Other options are incorrect because:

• a) The first pregnancy is rarely affected.

• c) It is not typically fatal.

• d) ABO incompatibility is independent and usually mild if present.

• IgG antibodies are the only class that can cross the placenta from mother to fetus.

• In HDFN, maternal IgG antibodies bind to fetal red blood cells carrying the corresponding antigen, leading to hemolysis.

Other antibody classes:

• IgM: Cannot cross the placenta; usually causes transfusion reactions, not HDFN.

• IgA: Found in mucosal secretions; does not cross placenta.

• IgD: Primarily a B-cell receptor; not involved in HDFN.

• Rh immune globulin (RhIG) is derived from pooled plasma of human donors who have high titers of anti-D antibodies.

• It contains IgG anti-D, which can bind fetal Rh-positive red cells in an Rh-negative mother, preventing sensitization.

Other options are incorrect because:

• b) Recombinant anti-D antibody: Currently, RhIG is not produced recombinantly.

• c) Fetal cord plasma: Not used to prepare RhIG.

• d) Artificial monoclonal IgM: RhIG requires IgG, not IgM, because IgG crosses the placenta.

DNA arrays (or microarrays) for blood group genotyping detect single nucleotide polymorphisms (SNPs) and other small genetic variations that differentiate blood group alleles.

• Stop codons (a) — not the primary target; some blood group changes involve stop codons, but arrays detect a broader range of SNPs.

• mRNA (b) — arrays use DNA, not mRNA, for genotyping.

• cDNA (d) — cDNA is used in some molecular methods, but standard blood group DNA arrays target genomic DNA SNPs.

• Platelet viability during storage is strongly influenced by the pH of the storage medium.

• If pH drops below ~6.2, platelets become nonfunctional and are ineffective for transfusion.

• Factors affecting pH include:

  • Platelet metabolism (produces lactic acid)

  • Gas exchange in storage bags

• Plasma potassium (a) rises during storage but does not directly reflect platelet function.

• PT (c) and aPTT (d) are coagulation tests, not indicators of platelet viability.

• Gel technology uses a dextran acrylamide gel matrix in a microtube containing anti-human globulin (AHG).

• Red cells that are agglutinated are trapped in the gel, while unagglutinated cells form a button at the bottom.

• Because the AHG is in the gel, no manual washing of cells is needed — eliminating the wash phase required in tube-based AHG testing.

• The other options are incorrect:

  • b) Centrifugation is required in gel testing.

  • c) Special equipment (gel centrifuge, incubator) is required.

  • d) Precise volumes of serum and cells are required.

• Exchange transfusion is a therapeutic procedure used in severe HDFN or hyperbilirubinemia.

• It works by:

  • Removing maternal antibody-coated red cells from the neonate’s circulation.

  • Reducing circulating bilirubin, thereby preventing kernicterus (bilirubin-induced neurological damage).

• The procedure may also help correct anemia and improve oxygen-carrying capacity.

Other options are incorrect because:

• b) Increasing plasma volume is a secondary effect, not the main purpose.

• c & d) Electrolytes and nutrients are not the primary targets of exchange transfusion.

• Intravenous RhIG is used in situations where there is a significant volume of fetal Rh-positive red cells in maternal circulation.

• This includes:

  • Large fetomaternal hemorrhage

  • Accidental transfusion of Rh-positive blood to an Rh-negative recipient

• IV administration allows rapid and complete neutralization of D-positive red cells.

Other options are incorrect because:

• b) Every pregnancy: Routine prophylaxis is usually given intramuscularly, not IV.

• c) ABO incompatibility: RhIG is irrelevant.

• d) Maternal anemia: RhIG does not treat anemia.

• The indirect antiglobulin test (IAT) relies on proper centrifugation to bring sensitized red cells into contact and allow agglutination.

• Under-centrifugation:

  • Cells are not packed sufficiently

  • Weak or small agglutinates may remain suspended
    → Leading to a false-negative reaction.

Why the others are less likely:

• b) Over-centrifugation → Can cause false-positive or overly compact cells, but not typically a false-negative.

• c) Dirty glassware → Can cause spurious agglutination (false positives).

• d) Use of EDTA plasma → Generally acceptable; EDTA prevents clotting and doesn’t usually cause false negatives in IAT.

• Severe Rh-mediated HDFN can cause extensive fetal anemia, leading to high-output cardiac failure.

• This results in hydrops fetalis, characterized by:

  • Generalized edema

  • Ascites

  • Pleural and pericardial effusions

• If untreated, it can be fatal in utero.

Other options are incorrect because:

• b) Mild anemia: Occurs in mild cases, not severe HDFN.

• c) Iron overload: Not caused by HDFN; occurs with repeated transfusions.

• d) Hypocalcemia: Not a direct consequence of Rh HDFN.

• The calibration test showed optimal results at 20 seconds:

  • Clear supernatant

  • Easy resuspension of red cells

  • Graded reaction strength of 1+ (which is within the acceptable range for IAT or DAT)

• Since 20 seconds gave the desired outcome, that is the time that should be set for routine use.

• Shorter time (15 seconds) might cause insufficient centrifugation; longer times (25–30 seconds) could cause stronger reactions or difficult resuspension, which is not optimal.

• AABB Standards require that each unit of cryoprecipitated anti-hemophilic factor (AHF) contains a minimum of 80 IU of Factor VIII at the time of issue.

• This ensures that therapeutic doses are delivered for patients with hemophilia A or other Factor VIII deficiencies.

Other options:

• 60, 70, 90 IU → either below or above the minimum standard; 80 IU is the established minimum.

Blood may be returned to inventory only if:

• The container closure is intact (not disturbed).

• At least one sealed segment remains attached for testing purposes.

• The unit has been maintained at the proper temperature throughout.

There is no strict requirement that the unit must be absent for less than 30 minutes—the key is temperature maintenance. The “30 minutes” rule is sometimes mentioned for platelet or RBC storage outside controlled conditions, but it is not a universal criterion for returning units to inventory.

• In an elution procedure, the goal is to remove (elute) antibody from red cells.

• The last wash is tested to ensure all unbound antibody has been washed out.

• If the last wash is nonreactive, it confirms that any antibody detected in the eluate came from the red cell surface (not leftover plasma/serum).

• If the last wash is reactive, the elution must be repeated after additional washing.

• Exchange transfusion blood must:

  • Be Group O to prevent ABO incompatibility reactions.

  • Be Rh-negative to avoid further sensitization or hemolysis.

  • Be crossmatch compatible with maternal serum, because maternal antibodies may still be present in the neonate and could react with donor red cells.

• The blood is usually fresh, irradiated, leukocyte-reduced, and CMV-safe.

Other options are incorrect because:

• b) Group-specific and Rh positive: Could trigger hemolysis if maternal antibodies are present.

• c) Group AB: AB red cells are not universal donor; plasma would contain anti-A or anti-B antibodies.

• d) Platelet-rich plasma: Does not provide red cells needed for exchange transfusion.

• CD34+ cell enumeration by flow cytometry is the most widely accepted and standardized quality control test to predict engraftment potential in hematopoietic progenitor cell (HPC) products.

• It provides a quantitative measure of the stem/progenitor cell content and correlates well with time to engraftment.

• Clonogenic assays (a) measure colony-forming units but take 1–2 weeks and are less practical for routine pre-transplant QC.

• Cell viability (b) is important but does not specifically measure the progenitor cell population.

• Manual differential (d) cannot identify CD34+ progenitor cells accurately.

• AHG (Anti-Human Globulin) control cells, also called check cells, are red blood cells coated with IgG and/or complement (C3).

• They are used as a positive control to verify that the anti-human globulin reagent is working properly, especially for anti-C3 reagents.

• They are not limited to the indirect antiglobulin test; they are used in both direct and indirect antiglobulin tests.

• They are coated with IgG and/or complement, not just IgG.

• They do not need to be used to confirm all positive reactions—only to check that the AHG reagent is functioning correctly when a negative reaction occurs.

• Middle cerebral artery (MCA) Doppler ultrasound is the first noninvasive indicator of fetal anemia.

• In anemic fetuses:

  • Blood viscosity decreases.

  • Blood flow velocity in the MCA increases, which can be measured by Doppler.

• This method is preferred over invasive procedures like amniocentesis unless intervention is required.

Other options are incorrect because:

• b) Ultrasound only: Standard ultrasound can detect structural changes but not early anemia.

• c) Amniocentesis: Previously used (spectrophotometry of bilirubin) but now reserved for confirmatory or therapeutic purposes.

• d) Fetal heart rate: Changes may occur late and are nonspecific.

• Anti-D (RhD antibody) is the most common cause of severe Hemolytic Disease of the Fetus and Newborn (HDFN) because:

  • The D antigen is highly immunogenic.

  • Sensitization of an Rh-negative mother carrying an Rh-positive fetus can lead to strong IgG antibody production.

  • These antibodies readily cross the placenta and cause significant hemolysis in the fetus.

Other antibodies:

• Anti-K (Kell) can cause severe HDFN but is less common.

• Anti-E usually causes mild HDFN.

• Anti-Fyᵃ (Duffy) rarely causes severe disease.

• In ABO hemolytic disease of the newborn (HDFN):

  • Maternal IgG antibodies against A or B antigens bind to fetal red cells.

  • However, fetal red cells express fewer ABO antigens, so the reaction is usually weak.

  • Therefore, the Direct Antiglobulin Test (DAT) is often weakly positive or sometimes even negative.

Other options are incorrect because:

• b) Strongly positive: Typical of Rh-mediated HDFN, not ABO.

• c) Always negative: DAT can be positive, just weakly.

• d) Uninterpretable: DAT results are interpretable; weak positivity is characteristic.

• AABB Standards require that apheresis platelet units be tested to ensure adequate platelet quality at the time of issue.

• Specifically, with 95% confidence, >95% of units must have a pH ≥ 6.2 at issue.

• This ensures platelets are viable and functional for transfusion.

Other options:

• 6.0 → too low; platelets may be nonfunctional.

• 6.8 or 7.0 → ideal physiologic pH, but not the minimum standard for release per AABB.

• Rh immune globulin (RhIG) works prophylactically by binding to any fetal Rh(D)-positive red cells that enter the maternal circulation.

• This prevents the mother’s immune system from recognizing and forming anti-D antibodies, thereby reducing the risk of HDFN in future pregnancies.

Other options are incorrect because:

• b) RhIG does not treat antibodies already formed; it is preventive.

• c) It does not enhance the immune response; it suppresses sensitization.

• d) RhIG is only effective in Rh-negative mothers, not Rh-positive.

• The Liley graph is used in amniocentesis to assess the severity of hemolytic disease of the fetus and newborn (HDFN).

• It plots optical density of amniotic fluid at 450 nm (reflecting bilirubin concentration) against gestational age.

• Based on the zone in the graph, clinicians can classify HDFN as mild, moderate, or severe, guiding management decisions.

Other options are incorrect because:

• b) Liley graph does not relate maternal antibody titer to fetal age.

• c) It does not plot hemoglobin.

• d) Antibody strength is not plotted against bilirubin in this graph.

• Chloroquine diphosphate is used to dissociate IgG from red blood cells without damaging most blood group antigens. This allows phenotyping of cells that are coated with IgG in a positive DAT.

• Bromelin (a) is an enzyme used to enhance antibody reactivity, not to remove IgG coating.

• LISS (c) is used to enhance antibody binding in serological testing, not to strip antibodies.

• DTT (d) is used to disrupt IgM antibodies by breaking disulfide bonds, and it can destroy some antigens (like Kell), so it is not generally used for this purpose.

• A positive Kleihauer–Betke (KB) test means that fetal red blood cells are present in the maternal circulation, indicating fetomaternal hemorrhage.

• This can occur due to:

  • Delivery

  • Trauma

  • Invasive procedures during pregnancy

  • Miscarriage or abortion

Other options are incorrect because:

• b) Maternal anemia: KB test does not measure maternal red cell quantity.

• c) ABO incompatibility: KB test does not detect antibodies or incompatibility.

• d) Infection: Irrelevant to KB test results.

Check cells (IgG-coated red cells) must agglutinate if the antiglobulin test was performed correctly.
No agglutination after adding them means the anti-IgG in the AHG reagent was unavailable — often because too few check cells were added to demonstrate agglutination.
Overwashing (a) would cause a false negative crossmatch but shouldn’t affect check cells; (b) and (c) are less likely here.

• HDFN is caused by maternal IgG antibodies directed against fetal red cell antigens (most commonly anti-D, but also anti-K, anti-c, etc.).

• These antibodies cross the placenta and cause hemolysis of fetal red blood cells.

• The other options are incorrect:

  • b) Fetal antibodies do not cause HDFN; the fetus does not typically produce significant antibodies against maternal RBCs in utero.

  • c) The fetus being Rh negative would not cause HDFN (in fact, if both mother and fetus are Rh negative, there’s no Rh D antigen to drive anti-D HDFN).

  • d) ABO incompatibility alone is not the definition — HDFN can occur with other antibodies, and ABO HDFN is usually milder and doesn’t always fit the full classic severe HDFN picture.

After repairs — especially those involving the lid, wiring, or motor — the centrifuge’s speed and timer accuracy must be checked to ensure it still provides the correct G-force and time for consistent test results.

• a) FDA reregistration is not required for a repaired lab instrument.

• b) Local board of health requalification is not standard for this type of repair.

• d) Using it immediately without verification could lead to erroneous test results.

• The Direct Antiglobulin Test (DAT), also called Coombs test, detects IgG antibodies or complement proteins already attached to red blood cells.

• In the context of HDFN, a positive DAT on cord blood indicates that maternal antibodies have bound to fetal red cells, which can lead to hemolysis.

Other options are incorrect because:

• b) Fetal hemoglobin is detected by other assays, not DAT.

• c) Bilirubin measurement is done via biochemical tests.

• d) ABO typing uses serologic or molecular methods, not DAT.

• Sensitization occurs when an Rh-negative mother is exposed to Rh-positive red blood cells. This exposure can happen through:

  • Pregnancy with an Rh-positive fetus (especially during delivery, miscarriage, or invasive procedures).

  • Transfusion of Rh-positive blood.

• Once sensitized, the mother can produce IgG anti-D antibodies, which may affect subsequent pregnancies.

Other options are incorrect:

• b) Infection with malaria: Does not cause Rh sensitization.

• c) Vitamin deficiency: Irrelevant.

• d) Platelet transfusion only: Platelets do not carry Rh antigens on a significant scale; this alone is not a common cause.

• ABO hemolytic disease of the newborn (HDN) occurs when the mother has antibodies (usually IgG anti-A or anti-B) against fetal ABO antigens.

• It is generally milder than Rh-mediated HDFN because:

  • Fetal red cells express fewer ABO antigens.

  • Maternal anti-A or anti-B antibodies are often partly IgM, which cannot cross the placenta.

• Most cases resolve without treatment, sometimes requiring only phototherapy.

Other options are incorrect:

• a) ABO HDN is less severe than Rh disease.

• c) It is rarely fatal.

• d) Anti-E is unrelated; it is an Rh system antibody.

• If the fetal screen (rosette test) is positive, it indicates that fetal D-positive red cells are present in the maternal circulation.

• The next step is the Kleihauer–Betke (KB) test, which quantifies the volume of fetomaternal hemorrhage.

• This quantification is essential to calculate the appropriate additional dose of RhIG to prevent maternal sensitization.

Other options are incorrect because:

• b) Indirect Coombs test: Detects maternal antibodies, not fetal cells.

• c) Rh typing: The fetus is already assumed D-positive if the screen is positive.

• d) DAT: Detects antibodies on fetal red cells, not the amount of fetal cells in maternal blood.

• The indirect antiglobulin test (IAT) detects IgG antibodies bound to red cells in vitro.

• Too heavy a cell suspension can cause:

  • Insufficient antibody per cell ratio

  • Impaired agglutination
    → Leading to a false-negative result.

Why the others are incorrect:

• a) Over-reading → would cause false positives, not negatives.

• b) IgG-coated screening cells → that’s normal; wouldn’t cause false negatives.

• c) Extra serum → generally increases the antibody-to-cell ratio; unlikely to cause false negatives.

AABB Standards require that apheresis platelet collections shall be shown to contain ≥ 3.0 × 10¹¹ platelets in > 75% of units tested, with 95% confidence.

This ensures adequate platelet dose for therapeutic efficacy.

• a) 5.5 × 10¹⁰ and b) 6.5 × 10¹⁰ are far too low for an apheresis unit.

• d) 5.0 × 10¹¹ is above the required minimum; the standard is 3.0 × 10¹¹.

• AABB Standards specify that platelets prepared from whole blood (also called pooled or random donor platelets) must contain ≥5.5 × 10¹⁰ platelets per unit in at least 90% of units tested.

• This ensures therapeutic efficacy when transfused to patients.

Other options:

• 6.5 × 10¹⁰ → minimum for apheresis platelets, not whole blood–derived.

• 7.5 × 10¹⁰ or 8.5 × 10¹⁰ → exceed the standard; not required for QC.

• Rh immune globulin (RhIG) is most effective when given within 72 hours postpartum to an Rh-negative mother who delivered an Rh-positive baby.

• This timing helps prevent maternal sensitization to the D antigen and reduces the risk of HDFN in future pregnancies.

Other options are incorrect because:

• b) RhIG is not needed if the infant is Rh-negative.

• c) Giving it before delivery only is insufficient; postpartum administration is critical.

• d) RhIG is preventive, given even if the antibody screen is negative.